FCPS Part1 Q BANK~Physiology Flash Cards~Very Important for Part 1

7/29/2019 FCPS Part1 Q BANK~Physiology Flash Cards~Very Important for Part 1

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Table 1 5 The Principal Lipoproteins.*

Composition (%)

Lipoprotein Size(nm) Protein FreeCholester

yl

Cholesterol Esters Triglyceride Phospholipid Origin

Chylomicrons

75 1000

2 2 3 90 3 Intestine

Chylomicron remnants

30 80 . . . . . . . . . . . . . . . Capillaries

Very lowdensitylipoproteins

(VLDL)

30 80 8 4 16 55 17 Liverandintestine

Intermediate-densitylipoproteins(IDL)

25 40 10 5 25 40 20 VLDL

Low-densitylipoproteins(LDL)

20 20 7 46 6 21 IDL

High-

densitylipoproteins(HDL)

7.5 10 50 4 16 5 25 Liver

andintestine

Table 3 3 Human Immunoglobulins.a

Immunoglobulin Function Heavy

Chain

Additional

Chain

Structure Plasma

Concentration

(mg/dL)

IgG Complement

activation

g1, g2,

g3, g4

Monomer 1000

IgA Localizedprotection inexternalsecretions(tears, intestinal

alpha 1,alpha2

J, SC Monomer;dimer with Jor SC chain;trimer with Jchain

200


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secretions, etc)

IgM Complementactivation

u J Pentamerwith J chain

120

IgD Antigen

recognition byB cells

dlta Monomer 3

IgE Reagin activity;releaseshistamine frombasophils andmast cells

e Monomer 0.05

Table 3 2 Examples of Cytokines and Their Clinical Relevance.

Cytokine Cellular

Sources

Major Activities Clinical Relevance

Interleukin-1 Macrophages Activation of T cells andmacrophages; promotionof inflammation

Implicated in thepathogenesis of septicshock, rheumatoid

arthritis, andatherosclerosis

Interleukin-2 Type 1 (TH1)helper T cells

Activation oflymphocytes, naturalkiller cells, andmacrophages

Used to inducelymphokine-activatedkiller cells; used in thetreatment of metastaticrenal-cell carcinoma,melanoma, and variousother tumors

Interleukin-4 Type 2 (TH2)

helper T cells,mast cells,basophils, andeosinophils

Activation of

lymphocytes, monocytes,and IgE class switching

As a result of its ability to

stimulate IgE production,plays a part in mast-cellsensitization and thus inallergy and in defenseagainst nematodeinfections

Interleukin-5 Type 2 (TH2)helper T cells,

Differentiation ofeosinophils

Monoclonal antibodyagainst interleukin-5 used


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mast cells, andeosinophils

to inhibit the antigen-induced late-phaseeosinophilia in animalmodels of allergy

Interleukin-6 Type 2 (TH2)

helper T cellsandmacrophages

Activation of

lymphocytes;differentiation of B cells;stimulation of theproduction of acute-phaseproteins

Overproduced in

Castleman's disease; actsas an autocrine growthfactor in myeloma and inmesangial proliferativeglomerulonephritis

Interleukin-8 T cells andmacrophages

Chemotaxis ofneutrophils, basophils,and T cells

Levels are increased indiseases accompanied byneutrophilia, making it apotentially useful markerof disease activity

Interleukin-11 Bone marrowstromal cells Stimulation of theproduction of acute-phaseproteins

Used to reducechemotherapy-inducedthrombocytopenia inpatients with cancer

Interleukin-12 Macrophagesand B cells

Stimulation of theproduction ofinterferon gyma by type 1(TH1) helper T cells andby natural killer cells;induction of type 1 (TH1)helper T cells

May be useful as anadjuvant for vaccines

Tumor necrosisfactor alpha

Macrophages,natural killercells, T cells, Bcells, and mastcells

Promotion ofinflammation

Treatment with antibodiesagainst tumor necrosisfactor -alpha beneficial inrheumatoid arthritis

Lymphotoxin(tumor necrosisfactor beta)

Type 1 (TH1)helper T cellsand B cells

Promotion ofinflammation

Implicated in thepathogenesis of multiplesclerosis and insulin-dependent diabetesmellitus

Transforminggrowth factorbeta

T cells,macrophages, Bcells, and mastcells

Immunosuppression May be useful therapeuticagent in multiple sclerosisand myasthenia gravis

Granulocyte-macrophagecolony-

T cells,macrophages,natural killer

Promotion of the growthof granulocytes andmonocytes

Used to reduceneutropenia afterchemotherapy for tumors


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stimulatingfactor

cells, and Bcells

and in ganciclovir-treatedpatients with AIDS; usedto stimulate cellproduction after bonemarrow transplantation

Interferon-alpha

Virally infectedcells

Induction of resistance ofcells to viral infection

Used to treat AIDS-related Kaposi sarcoma,melanoma, chronichepatitis B infection, andchronic hepatitis Cinfection

Interferon-beta Virally infectedcells

Induction of resistance ofcells to viral infection

Used to reduce thefrequency and severity ofrelapses in multiplesclerosis

Interferon-gyma Type 1 (TH1)helper T cells

and naturalkiller cells

Activation ofmacrophages; inhibitionof type 2 (TH2) helper Tcells

Used to enhance thekilling of phagocytosedbacteria in chronicgranulomatous disease

Table 4 1 Nerve Fiber Types in Mammalian Nerve.a

Fiber Type Function Fiber

Diameter

(um)

Conduction

Velocity

(m/s)

Spike

Duration

(ms)

Absolute

Refractory

Period (ms)

A

alpha Proprioception;somatic motor

12 20 70 120

beta Touch, pressure 5 12 30 70 0.4 0.5 0.4 1

gyma Motor to musclespindles

3 6 15 30

delta Pain, cold, touch 2 5 12 30


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B Preganglionicautonomic


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Small-Molecule

Transmitter

Neuropeptide

Monoamines

Acetylcholine Enkephalin, calcitonin-gene-related peptide, galanin,

gonadotropin-releasing hormone, neurotensin, somatostatin,substance P, vasoactive intestinal polypeptide

Serotonin Cholecystokinin, enkephalin, neuropeptide Y, substance P,vasoactive intestinal polypeptide

Catecholamines

Dopamine Cholecystokinin, enkephalin, neurotensin

Norepinephrine Enkephalin, neuropeptide Y, neurotensin, somatostatin,vasopressin

Epinephrine Enkephalin, neuropeptide Y, neurotensin, substance P

Amino AcidsGlutamate Substance P

Glycine Neurotensin

GABA Cholecystokinin, enkephalin, somatostatin, substance P,thyrotropin-releasing hormone

Table 18 4 Temperature-Regulating Mechanisms.

Mechanisms activated by cold

Shivering

Hunger

Increased voluntary activity

Increased secretion of norepinephrine and epinephrine

Decreased heat loss

Cutaneous vasoconstriction

Curling up

Horripilation

Mechanisms activated by heat

Increased heat loss

Cutaneous vasodilation

Sweating


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Increased respiration

Decreased heat production

Anorexia

Apathy and inertia

Table 19 1 Aphasias. Characteristic Responses of Patients with Lesions in VariousAreas When Shown a Picture of a Chair.

Type of Aphasia and Site of Lesion Characteristic Naming ErrorsNonfluent (Broca s area) "Tssair"

Fluent (Wernicke s area) "Stool" or "choss" (neologism)

Fluent (areas 40, 41, and 42; conductionaphasia)

"Flair . . . no, swair . . . tair."

Anomic (angular gyrus) "I know what it is . . . I have a lot ofthem."

Table 20 2 Effect of Variations in the Concentrations of Thyroid Hormone-BindingProteins in the Plasma on Various Parameters of Thyroid Function after Equilibrium HasBeen Reached.

Condition Concentrations

of Binding

Proteins

Total

Plasma

T4, T3,

RT3

Free

Plasma

T4, T3,

RT3

Plasma

TSH

Clinical

State

Hyperthyroidism Normal High High Low Hyperthyroid

Hypothyroidism Normal Low Low High Hypothyroid

Estrogens,methadone, heroin,major tranquilizers,clofibrate

High High Normal Normal Euthyroid

Glucocorticoids, Low Low Normal Normal Euthyroid


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androgens, danazol,asparaginase

Table 20 3 Causes of Congenital Hypothyroidism.

Maternal iodine deficiency

Fetal thyroid dysgenesis

Inborn errors of thyroid hormone synthesis

Maternal antithyroid antibodies that cross the placenta

Fetal hypopituitary hypothyroidism

Table 20 4 Causes of Hyperthyroidism.

Thyroid overactivity

Solitary toxic adenomaToxic multinodular goiter

Hashimoto thyroiditis

TSH-secreting pituitary tumor

Mutations causing constitutive activation of TSH receptor

Other rare causes

Extrathyroidal

Administration of T3 or T4 (factitious or iatrogenic hyperthyroidism)

Ectopic thyroid tissue

Table 20 5 Physiologic Effects of Thyroid Hormones.


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Target

Tissue

Effect Mechanism

Heart ChronotropicInotropic

Increased number of -beta-adrenergic receptors

Enhanced responses to circulating catecholamines

Increased proportion of -alpha-myosin heavy chain(with higher ATPase activity)

Adiposetissue

Catabolic Stimulated lipolysis

Muscle Catabolic Increased protein breakdown

Bone Developmental Promote normal growth and skeletal development

Nervoussystem

Developmental Promote normal brain development

Gut Metabolic Increased rate of carbohydrate absorption

Lipoprotein Metabolic Formation of LDL receptorsOther Calorigenic Stimulated oxygen consumption by metabolically

active tissues (exceptions: testes, uterus, lymph nodes,spleen, anterior pituitary)

Increased metabolic rate

Table 21 2 Substances with Insulin-Like Activity in Human Plasma.

Insulin

Proinsulin

Nonsuppressible insulin-like activity (NSILA)

Low-molecular-weight fractionIGF-I

IGF-II

High-molecular-weight fraction (mostly IGF bound to protein)


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Table 21 3 Principal Actions of Insulin.

Rapid (seconds)

Increased transport of glucose, amino acids, and K

+

into insulin-sensitive cells

Intermediate (minutes)

Stimulation of protein synthesis

Inhibition of protein degradation

Activation of glycolytic enzymes and glycogen synthase

Inhibition of phosphorylase and gluconeogenic enzymes

Delayed (hours)

Increase in mRNAs for lipogenic and other enzymes

Table 21 4 Effects of Insulin on Various Tissues.

Adipose tissue

Increased glucose entry

Increased fatty acid synthesis

Increased glycerol phosphate synthesis

Increased triglyceride deposition

Activation of lipoprotein lipase

Inhibition of hormone-sensitive lipase

Increased K+ uptake

MuscleIncreased glucose entry

Increased glycogen synthesis

Increased amino acid uptake

Increased protein synthesis in ribosomes

Decreased protein catabolism


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Decreased release of gluconeogenic amino acids

Increased ketone uptake

Increased K+ uptake

LiverDecreased ketogenesis

Increased protein synthesis

Increased lipid synthesis

Decreased glucose output due to decreased gluconeogenesis, increased glycogensynthesis, and increased glycolysis

General

Increased cell growth

Table 21 5 Glucose Transporters in Mammals.

Function Km

(mM)a

Major Sites of

Expression

Secondary active

transport (Na1-

glucose cotransport)

SGLT 1 Absorption of glucose 0.1 1.0 Small intestine, renaltubules

SGLT 2 Absorption of glucose 1.6 Renal tubules

Facilitated diffusion

GLUT 1 Basal glucose uptake 1 2 Placenta, blood-brain

barrier, brain, red cells,kidneys, colon, many otherorgans

GLUT 2 B-cell glucose sensor;transport out of intestinaland renal epithelial cells

12 20 B cells of islets, liver,epithelial cells of smallintestine, kidneys

GLUT 3 Basal glucose uptake


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many other organs

GLUT 4 Insulin-stimulatedglucose uptake

5 Skeletal and cardiacmuscle, adipose tissue,other tissues

GLUT 5 Fructose transport 1 2 Jejunum, spermGLUT 6 None Pseudogene

GLUT 7 Glucose 6-phosphateransporter in endoplasmicreticulum

Liver, ? other tissues

Table 21 6 Factors Affecting Insulin Secretion.

Stimulators Inhibitors

Glucose Somatostatin

Mannose 2-Deoxyglucose

Amino acids (leucine, arginine, others) Mannoheptulose

Intestinal hormones (GIP, GLP-1 [7 36],gastrin, secretin, CCK; others?)

alpha-Adrenergic stimulators(norepinephrine, epinephrine)

beta-Keto acids beta-Adrenergic blockers (propranolol)

Acetylcholine

Glucagon GalaninCyclic AMP and various cAMP-generatingsubstances

Diazoxide

Thiazide diuretics

beta-Adrenergic stimulators K+ depletion

Theophylline Phenytoin

Sulfonylureas Alloxan

Microtubule inhibitors

Insulin


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Table 21 8 Factors Affecting Glucagon Secretion.

Stimulators Inhibitors

Amino acids (particularly the glucogenic amino acids: alanine,serine, glycine, cysteine, and threonine) Glucose

CCK, gastrin Somatostatin

Cortisol Secretin

Exercise FFA

Infections Ketones

Other stresses Insulin

beta-Adrenergic stimulators Phenytoin

Theophylline alpha-Adrenergic

stimulatorsAcetylcholine GABA

Table 22 4 Typical Effects of Cortisol on the White and Red Blood Cell Counts in

Humans (Cells/ L).

Cell Normal Cortisol-Treated

White blood cells

Total 9000 10,000

PMNs 5760 8330

Lymphocytes 2370 1080

Eosinophils 270 20

Basophils 60 30

Monocytes 450 540

Red blood cells 5 million 5.2 million

Table 22 5 Typical Plasma Electrolyte Levels in Normal Humans and Patients withAdrenocortical Diseases.

Plasma Electolytes (mEq/L)


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State Na+

K+

Cl

HCO3

Normal 142 4.5 105 25

Adrenal insufficiency 120 6.7 85 25

Primary hyperaldosteronism 145 2.4 96 41

Table 22 6 Conditions that Increase Aldosterone Secretion.

Glucocorticoid secretion also increasedSurgery

Anxiety

Physical trauma

Hemorrhage

Glucocorticoid secretion unaffected

High potassium intake

Low sodium intake

Constriction of inferior vena cava in thoraxStanding

Secondary hyperaldosteronism (in some cases of congestive heart failure, cirrhosis, andnephrosis)

Table 22 7 Second Messengers Involved in the Regulation of Aldosterone Secretion.

Secretagogue Intracellular Mediator

ACTH Cyclic AMP, protein kinase A

Angiotensin II Diacylglycerol, protein kinase C

K+ Ca + via voltage-gated Ca + channels


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Table 24 3 Stimuli that Affect Growth Hormone Secretion in Humans.

Stimuli that increase secretion

Hypoglycemia

2-Deoxyglucose

Exercise

Fasting

Increase in circulating levels of certain amino acids

Protein meal

Infusion of arginine and some other amino acids

Glucagon

Stressful stimuli

Pyrogen

Lysine vasopressin

Various psychologic stresses

Going to sleep

L-Dopa and alpha-adrenergic agonists that penetrate the brain

Apomorphine and other dopamine receptor agonists

Estrogens and androgens

Stimuli that decrease secretion

REM sleep

Glucose

Cortisol

FFA

Medroxyprogesterone

Growth hormone and IGF-I


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Table 25 3 Factors Affecting the Secretion of Human Prolactin and Growth Hormone.

Factor Prolactina

Growth Hormonea

Sleep I+ I+

Nursing I++ N

Breast stimulation in nonlactating women I N

Stress I+ I+

Hypoglycemia I I+

Strenuous exercise I I

Sexual intercourse in women I N

Pregnancy I++ N

Estrogens I I

Hypothyroidism I N

TRH I+ N

Phenothiazines, butyrophenones I+ N

Opioids I I

Glucose N D

Somatostatin N D+

L-Dopa D+ I+

Apomorphine D+ I+

Bromocriptine and related ergot derivatives D+ I

aI, moderate increase; I+, marked increase; I++, very marked increase; N, no change; D,moderate decrease; D+, marked decrease; TRH, thyrotropin-releasing hormone.

Table 25 7 Twenty-Four-Hour Production Rates of Sex Steroids in Women at DifferentStages of the Menstrual Cycle.


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Sex Steroids Early Follicular Preovulatory Midluteal

Progesterone (mg) 1.0 4.0 25.0

17-hydroxyprogesterone (mg) 0.5 4.0 4.0

Dehydroepiandrosterone (mg) 7.0 7.0 7.0

Androstenedione (mg) 2.6 4.7 3.4

Testosterone (ug) 144.0 171.0 126.0

Estrone (ug) 50.0 350.0 250.0

Estradiol (ug) 36.0 380.0 250.0

Table 25 9 Hormone Levels in Human Maternal Blood during Normal Pregnancy.

Hormone Approximate Peak Value Time of Peak Secretion

hCG 5 mg/mL First trimester

Relaxin 1 ng/mL First trimester

hCS 15 mg/mL Term

Estradiol 16 ng/mL Term

Estriol 14 ng/mL Term

Progesterone 190 ng/mL Term

Prolactin 200 ng/mL Term

Table 25 10 Composition of Colostrum and Milk.*

Component Human Colostrum Human Milk Cows' Milk

Water, g . . . 88 88

Lactose, g 5.3 6.8 5.0


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Protein, g 2.7 1.2 3.3

Casein: lactalbumin ratio . . . 1:2 3:1

Fat, g 2.9 3.8 3.7

Linoleic acid . . . 8.3% of fat 1.6% of fat

Sodium, mg 92 15 58

Potassium, mg 55 55 138

Chloride, mg 117 43 103

Calcium, mg 31 33 125

Magnesium, mg 4 4 12

Phosphorus, mg 14 15 100

Iron, mg 0.09 0.15a 0.10a

Vitamin A, ug 89 53 34Vitamin D, ug . . . 0.03a 0.06a

Thiamine, ug 15 16 42

Riboflavin, ug 30 43 157

Nicotinic acid, ug 75 172 85

Ascorbic acid, mg 4.4a 4.3a 1.6a

Table 26 1 Contents of Normal Gastric Juice (Fasting State).

Cations: Na+, K+, Mg +, H+ (pH approximately 1.0)

Anions: Cl , HPO4 , SO4

Pepsins

Lipase

Mucus

Intrinsic factor


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Table 26 2 Principal Digestive Enzymes.*

Source Enzyme Activator Substrate Catalytic

Function orProducts

Salivaryglands

Salivary alpha-amylase

Cl Starch Hydrolyzes 1:4-alpha linkages,producing -alpha-limit dextrins,maltotriose, andmaltose

Lingualglands

Lingual lipase Triglycerides Fatty acids plus1,2-diacylglycerols

Stomach Pepsins(pepsinogens)

HCl Proteins andpolypeptides

Cleave peptidebonds adjacent toaromatic aminoacids

Gastric lipase Triglycerides Fatty acids andglycerol

Exocrinepancreas

Trypsin (trypsinogen) Enteropeptidase Proteins andpolypeptides

Cleave peptidebonds on carboxylside of basic aminoacids (arginine or

lysine)Chymotrypsins(chymotrypsinogens)

Trypsin Proteins andpolypeptides

Cleave peptidebonds on carboxylside of aromaticamino acids

Elastase (proelastase) Trypsin Elastin, someother proteins

Cleaves bonds oncarboxyl side ofaliphatic aminoacids

Carboxypeptidase A

(procarboxypeptidaseA)

Trypsin Proteins and

polypeptides

Cleave carboxyl

terminal aminoacids that havearomatic orbranched aliphaticside chains

Carboxypeptidase B(procarboxypeptidase

Trypsin Proteins andpolypeptides

Cleave carboxylterminal amino


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B) acids that havebasic side chains

Colipase(procolipase)

Trypsin Fat droplets Facilitatesexposure of activesite of

pancreaticlipasePancreatic lipase . . . Triglycerides Monoglycerides

and fatty acids

Bile salt-acid lipase Cholesterylesters

Cholesterol

Cholesteryl esterhydrolase

. . . Cholesterylesters

Cholesterol

Pancreatic alpha-amylase

Cl Starch Same as salivary -alpha-amylase

Ribonuclease . . . RNA NucleotidesDeoxyribonuclease . . . DNA Nucleotides

Phospholipase A2(pro-phospholipaseA2)

Trypsin Phospholipids Fatty acids,lysophospholipids

Intestinalmucosa

Enteropeptidase . . . Trypsinogen Trypsin

Aminopeptidases . . . Polypeptides Cleave aminoterminal aminoacid from peptide

Carboxypeptidases . . . Polypeptides Cleave carboxylterminal aminoacid from peptide

Endopeptidases . . . Polypeptides Cleave betweenresidues inmidportion ofpeptide

Dipeptidases . . . Dipeptides Two amino acids

Maltase . . . Maltose,maltotriose,alpha-dextrins

Glucose

Lactase . . . Lactose Galactose andglucose

Sucrasea . . . Sucrose; alsomaltotriose

Fructose andglucose


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and maltose

alpha-Dextrinasea . . . alpha-Dextrins,maltosemaltotriose

Glucose

Trehalase . . . Trehalose Glucose

Nuclease and relatedenzymes

. . . Nucleic acids Pentoses andpurine andpyrimidine bases

Cytoplasmof mucosalcells

Various peptidases . . . Di-, tri-, andtetrapeptides

Amino acids

*Corresponding proenzymes, where relevant, are shown in parentheses

aSucrase and a-dextrinase are separate subunits of a single protein

Table 26 5 Daily Water Turnover (mL) in the Gastrointestinal Tract.

Ingested 2000

Endogenous secretions 7000

Salivary glands 1500

Stomach 2500

Bile 500

Pancreas 1500

Intestine +1000

=7000Total input 9000

Reabsorbed 8800

Jejunum 5500

Ileum 2000

Colon +1300


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=8800

Balance in stool 200

Table 26 7 Stimuli that Affect Gastrin Secretion.

Stimuli that increase gastrin secretion

Luminal

Peptides and amino acids

Distention

Neural

Increased vagal discharge via GRP

BloodborneCalcium

Epinephrine

Stimuli that inhibit gastrin secretion

Luminal

Acid

Somatostatin

Bloodborne

Secretin, GIP, VIP, glucagon, calcitonin

Table 27 1 Normal Transport of Substances by the Intestine and Location of

Maximum Absorption or Secretion.

a

Small Intestine

Absorption of: Upper Mid Lower Colon

Sugars (glucose, galactose, etc) ++ +++ ++ 0


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Amino acids ++ ++ ++ 0

Water-soluble and fat-soluble vitamins except vitaminB12

+++ ++ 0 0

Betaine, dimethylglycine, sarcosine + ++ ++ ?

Antibodies in newborns + ++ +++ ?Pyrimidines (thymine and uracil) + + ? ?

Long-chain fatty acid absorption and conversion totriglyceride

+++ ++ + 0

Bile acids + + +++

Vitamin B12 0 + +++ 0

Na+ +++ ++ +++ +++

K+ + + + Sec

Ca + +++ ++ + ?

Fe + +++ + + ?

Cl +++ ++ + +

SO4 ++ + 0 ?

Table 27 2 Factors Affecting the Metabolic Rate.

Muscular exertion during or just before measurement

Recent ingestion of food

High or low environmental temperature

Height, weight, and surface area


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Sex

Age

Growth

Reproduction

Lactation

Emotional state

Body temperature

Circulating levels of thyroid hormones

Circulating epinephrine and norepinephrine levels

Table 28 1 Mean Lengths of Various Segments of the Gastrointestinal Tract asMeasured by Intubation in Living Humans.

Segment Length (cm)

Pharynx, esophagus, and stomach 65

Duodenum 25

Jejunum and ileum 260

Colon 110

Table 29 1 Principal Functions of the Liver.

Formation and secretion of bileNutrient and vitamin metabolism

Glucose and other sugars

Amino acids

Lipids

Fatty acids


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Cholesterol

Lipoproteins

Fat-soluble vitamins

Water-soluble vitamins

Inactivation of various substances

Toxins

Steroids

Other hormones

Synthesis of plasma proteins

Acute-phase proteins

Albumin

Clotting factors

Steroid-binding and other hormone-binding proteinsImmunity

Kupffer cells

Table 30 1 Conduction Speeds in Cardiac Tissue.

Tissue Conduction Rate (m/s)

SA node 0.05Atrial pathways 1

AV node 0.05

Bundle of His 1

Purkinje system 4

Ventricular muscle 1


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Table 30 2 ECG Intervals.

Normal Durations

Intervals Average Range Events in the Heart during IntervalPR intervala 0.18 0.12 0.20 Atrial depolarization and conduction

through AV node

QRS duration 0.08 to 0.10 Ventricular depolarization and atrialrepolarization

QT interval 0.40 to 0.43 Ventricular depolarization plusventricular repolarization

ST interval (QTminus QRS)

0.32 . . . Ventricular repolarization (during Twave)

aMeasured from the beginning of the P wave to the beginning of the QRS complex.

bShortens as heart rate increases from average of 0.18 s at a rate of 70 beats/min to 0.14s at a rate of 130 beats/min.

Table 31 1 Variation in Length of Action Potential and Associated Phenomena withCardiac Rate.a

Heart Rate

75/min

Heart Rate

200/min

Skeletal

Muscle

Duration, each cardiac cycle 0.80 0.30 . . .

Duration of systole 0.27 0.16 . . .

Duration of action potential 0.25 0.15 0.007

Duration of absolute refractoryperiod

0.20 0.13 0.004

Duration of relative refractoryperiod 0.05 0.02 0.003

Duration of diastole 0.53 0.14 . . .


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Table 31 3 Effect of Various Conditions on Cardiac Output.

Condition or Factora

No change Sleep

Moderate changes in environmental temperature

Increase Anxiety and excitement (50 100%)

Eating (30%)

Exercise (up to 700%)

High environmental temperature

Pregnancy

Epinephrine

Decrease Sitting or standing from lying position (20 30%)

Rapid arrhythmias

Heart disease

Table 31 4 Changes in Cardial Function with Exercise. Note that Stroke VolumeLevels off, Then Falls Somewhat (as a Result of the Shortening of Diastole) When theHeart Rate Rises to High Values.

Work (kg-

m/min)

O2 Usage

(mL/min)

Pulse

Rate (per

min)

Cardiac

Output

(L/min)

Stroke

Volume

(mL)

A-V O2

Difference

(mL/dL)

Rest 267 64 6.4 100 4.3

288 910 104 13.1 126 7.0

540 1430 122 15.2 125 9.4

900 2143 161 17.8 110 12.3

1260 3007 173 20.9 120 14.5


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Table 32 1 Normal Values for the Cellular Elements in Human Blood.

CellCells/ L

(average)

Approximate Normal

Range

Percentage of Total

White Cells

Total white bloodcells

9000 4000 11,000 ...

Granulocytes

Neutrophils 5400 3000 6000 50 70

Eosinophils 275 150 300 1 4

Basophils 35 0 100 0.4

Lymphocytes 2750 1500 4000 20 40

Monocytes 540 300 600 2 8

ErythrocytesFemales 4.8 x 10 . . . . . .

Males 5.4 x 10 . . . . . .

Platelets 300,000 200,000 500,000 . . .

Table 33 1 Summary of Factors Affecting the Caliber of the Arterioles.

Constriction Dilation

Local factors


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Decreased local temperature Increased CO2 and decreased O2

Autoregulation Increased K+, adenosine, lactate, etc

Decreased local pHIncreased local temperature

Endothelial products

Endothelin-1 NO

Locally released platelet serotonin Kinins

Thromboxane A2 Prostacyclin

Circulating hormones

Epinephrine (except in skeletal

muscle and liver)

Epinephrine in skeletal muscle and liver

Norepinephrine CGRP alpha

AVP Substance P

Angiotensin II Histamine

Circulating Na+-K+ ATPaseinhibitor

ANP

Neuropeptide Y VIP

Neural factors

Increased discharge of sympatheticnerves

Decreased discharge of sympathetic nerves

Activation of sympathetic cholinergic vasodilatornerves to skeletal muscle

The terms vasoconstriction and vasodilation are generally used to refer to constriction and dilation ofthe resistance vessels. Changes in the caliber of the veins are referred to specifically asvenoconstrictionor venodilation.

Table 34 1 Resting Blood Flow and O2 Consumption of Various Organs in a 63-kgAdult Man with a Mean Arterial Blood Pressure of 90 mm Hg and an O2Consumption of 250 mL/min.


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Blood Flow Arteriove

nous

Oxygen

Difference

(mL/L)

Oxygen

Consumptio

n

Resistance

(R units)a

Percentage of

Total

Region Mass

(kg

)

mL/min mL/100

g/mi

n

mL/min mL/100

g/mi

n

Absolute perkg Cardiac

Outp

ut

OxygenConsump

tion

Liver 2.6 1500 57.7 34 51 2.0 3.6 9.4 27.8 20.4

Kidneys

0.3 1260 420.0 14 18 6.0 4.3 1.3 23.3 7.2

Brain 1.4 750 54.0 62 46 3.3 7.2 10.1

13.9 18.4

Skin 3.6 462 12.8 25 12 0.3 11.7 42.

1

8.6 4.8

Skeletalmuscle

31.0

840 2.7 60 50 0.2 6.4 198.4

15.6 20.0

Heartmuscle

0.3 250 84.0 114 29 9.7 21.4 6.4 4.7 11.6

Restof

body

23.8

336 1.4 129 44 0.2 16.1 383.2

6.2 17.6

Wholebody

63.0

5400 8.6 46 250 0.4 1.0 63.0

100.0 100.0

Table 34 2 Concentration of Various Substances in Human CSF and Plasma.

Substance CSF Plasma Ratio CSF/Plasma

Na+ (meq/kg H2O) 147.0 150.0 0.98

K+ (meq/kg H2O) 2.9 4.6 0.62

Mg + (meq/kg H2O) 2.2 1.6 1.39

Ca + (meq/kg H2O) 2.3 4.7 0.49


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Cl (meq/kg H2O) 113.0 99.0 1.14

HCO3 (meq/L) 25.1 24.8 1.01

PCO2 (mm Hg) 50.2 39.5 1.28

pH 7.33 7.40 . . .

Osmolality (mosm/kg H2O) 289.0 289.0 1.00

Protein (mg/dL) 20.0 6000.0 0.003

Glucose (mg/dL) 64.0 100.0 0.64

Inorganic P (mg/dL) 3.4 4.7 0.73

Urea (mg/dL) 12.0 15.0 0.80

Creatinine (mg/dL) 1.5 1.2 1.25Uric acid (mg/dL) 1.5 5.0 0.30

Cholesterol (mg/dL) 0.2 175.0 0.001

Table 34 4 Pressure in Aorta and Left and Right Ventricles (Vent) in Systole andDiastole.

Pressure (mm Hg) in Pressure Differential (mm Hg) between

Aorta and

Aorta Left

Vent

Right

Vent

Left Vent Right Vent

Systole 120 121 25 1 95

Diastole 80 0 0 80 80

Table 36 3 Plasma pH, HCO3 , and PCO2 Values in Various Typical Disturbances ofAcid-Base Balance.a

Arterial Plasma


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Condition pH HCO3

(mEq/L)

PCO2 (mm

Hg)

Cause

Normal 7.40 24.1 40

Metabolicacidosis 7.28 18.1 40 NH4 Cl ingestion

6.96 5.0 23 Diabetic acidosis

Metabolicalkalosis

7.50 30.1 40 NaHCO3 ingestion

7.56 49.8 58 Prolonged vomiting

Respiratoryacidosis

7.34 25.0 48 Breathing 7% CO2

7.34 33.5 64 Emphysema

Respiratoryalkalosis 7.53 22.0 27 Voluntary hyperventilation7.48 18.7 26 Three-week residence at 4000-m altitude

aIn the diabetic acidosis and prolonged vomiting examples, respiratory compensationfor primary metabolic acidosis and alkalosis has occurred, and the Pco2 has shiftedfrom 40 mm Hg. In the emphysema and high-altitude examples, renal compensation forprimary respiratory acidosis and alkalosis has occurred and has made the deviationsfrom normal of the plasma HCO3

larger than they would otherwise be.

Table 38 3 Agents Causing Contraction or Relaxation of Mesangial Cells.

Contraction Relaxation

Endothelins ANPAngiotensin II Dopamine

Vasopressin PGE2

Norepinephrine cAMP

Platelet-activating factor

Platelet-derived growth factor


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Thromboxane A2

PGF2

Leukotrienes C4 and D4

Histamine

Table 38 6 Transport Proteins Involved in the Movement of Na+ and Cl Across theApical Membranes of Renal Tubular Cells.a

Site Apical Transporter Function

Proximal tubule Na/glucose CT Na+ uptake, glucose uptake

Na+/Pi CT Na+ uptake, Pi uptake

Na+ amino acid CT Na+ uptake, amino acid uptake

Na/lactate CT Na+ uptake, lactate uptake

Na/H exchanger Na+ uptake, H+ extrusion

Cl/base exchanger Cl uptake

Thick ascending limb Na K 2Cl CT Na+ uptake, Cl uptake, K+ uptake

Na/H exchanger Na

+

uptake, H

+

extrusion

K+ channels K+ extrusion (recycling)

Distal convoluted tubule NaCl CT Na+ uptake, Cl uptake

Collecting duct Na+ channel (ENaC) Na+ uptake


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aUptake indicates movement from tubular lumen to cell interior, extrusion is movementfrom cell interior to tubular lumen. CT, cotransporter; Pi, inorganic phosphate.

Table 38 8 Permeability and Transport in Various Segments of the Nephron.a

Permeability

H2O Urea NaCl Active Transport of Na+

Loop of Henle

Thin descending limb 4+ + 0

Thin ascending limb 0 + 4+ 0

Thick ascending limb 0 4+

Distal convoluted tubule 3+

Collecting tubule

Cortical portion 3+* 0 2+

Outer medullary portion 3+* 0 1+

Inner medullary portion 3+* 3+ 1+

Table 38 10 Mechanism of Action of Various Diuretics.

Agent Mechanism of Action

Water Inhibits vasopressin secretion.

Ethanol Inhibits vasopressin secretion.

Antagonists of V2 vasopressinreceptors such as astolvaptan

Inhibit action of vasopressin on collectingduct.


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Large quantities of osmotically activesubstances such as mannitol andglucose

Produce osmotic diuresis.

Xanthines such as caffeine andtheophylline

Decrease tubular reabsorption of Na+ andincrease GFR.

Acidifying salts such as CaCl2 andNH4Cl

Supply acid load; H+ is buffered, but an anionis excreted with Na+ when the ability of thekidneys to replace Na+ with H+ is exceeded.

Carbonic anhydrase inhibitors suchas acetazolamide (Diamox)

Decrease H+ secretion, with resultant increasein Na+ and K+ excretion.

Metolazone (Zaroxolyn), thiazidessuch as chlorothiazide (Diuril)

Inhibit the Na Cl cotransporter in the earlyportion of the distal tubule.

Loop diuretics such as furosemide(Lasix), ethacrynic acid (Edecrin),and bumetanide

Inhibit the Na K 2Cl cotransporter in themedullary thick ascending limb of the loop ofHenle

K+-retaining natriuretics such asspironolactone (Aldactone),triamterene (Dyrenium), andamiloride (Midamor)

Inhibit Na+ K+ "exchange" in the collectingducts by inhibiting the action of aldosterone(spironolactone) or by inhibiting the ENaCs(amiloride).

Table 39 1 Summary of Stimuli Affecting Vasopresson Secretion.

Vasopressin Secretion Increased Vasopressin Secretion Decreased

Increased effective osmotic pressure ofplasma

Decreased effective osmotic pressure ofplasma

Decreased ECF volume Increased ECF volume

Pain, emotion, "stress," exercise Alcohol

Nausea and vomiting

Standing


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Clofibrate, carbamazepine

Angiotensin II

Table 39 2 Factors that Affect Renin Secretion.

Stimulatory

Increased sympathetic activity via renal nerves

Increased circulating catecholamines

Prostaglandins

Inhibitory

Increased Na+ and Cl reabsorption across macula densa

Increased afferent arteriolar pressure

Angiotensin II

Vasopressin

Table 39 3 Conditions that Increase Renin Secretion.

Na+ depletion

Diuretics

Hypotension

Hemorrhage

Upright posture

Dehydration

Cardiac failure

Cirrhosis

Constriction of renal artery or aorta

Various psychologic stimuli


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Table 40 2 Principal Buffers in Body Fluids.

Blood H2CO3 H+ + HCO3

HProt H+ + Prot

HHb H+ + Hb

Interstitial fluid H2CO3 H+ + HCO3

Intracellular fluid HProt H+ + Prot

H2PO4 H+ + HPO4

2

Table 58 4 Comparison of Th-1 Cells and Th-2 Cells

Property Th-1

Cells

Th-2

Cells

Produces IL-2 and gamma interferon Yes No

Produces IL-4, IL-5, IL-6, and IL-10 No Yes

Enhances cell-mediated immunity and delayed hypersensitivityprimarily

Yes No

Enhances antibody production primarily No Yes

Stimulated by IL-12 Yes NoStimulated by IL-4 No Yes

Table 58 7 Important Functions of the Main Cytokines

Major Source Cytokine Important Functions


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Macrophages Interleukin-1 Proinflammatory cytokine. Induces fever.Induces liver to produce acute phase proteins.

Interleukin-6 Proinflammatory cytokine. Induces fever.Induces liver to produce acute phase proteins.

Tumor necrosisfactor Proinflammatory cytokine. Low concentration:activates neutrophils and increases theiradhesion to endothelial cells. Highconcentration: mediates septic shock, acts ascachectin, causes necrosis of tumors.

Interleukin-12 Drives development of Th-1 subset of T cells.

Th-1 subset ofhelper T cells

Interleukin-2 T-cell growth factor. Stimulates growth ofboth helper (CD4) and cytotoxic (CD8) Tcells.

Gamma

interferon

Stimulates phagocytosis and killing by

macrophages. Increases class I and II MHCprotein expression. Inhibits growth of Th-2cells.

Th-2 subset ofhelper T cells

Interleukin-4 Drives development of Th-2 subset of T cells.Stimulates B-cell growth. Increases isotypeclass switching to IgE.

Interleukin-5 Increases number of eosinophils. Increasesisotype class switching to IgA.

Interleukin-10 Antiinflammatory cytokine. Inhibitsdevelopment of Th1 subset of T cells.

Th-17 subset of Tcells

Interleukin-17 Recruits neutrophils to site of infection.Important in gut mucosal immunity.

Many cellsincludingmacrophages, Tcells, and B cells.

TransformingGrowth Factor-beta

Antiinflammatory cytokine. Inhibits activationof T cells. Increases isotype switching to IgA.

Table 59 1 Properties of Human Immunoglobulins

Property lgG lgA lgM lgD lgE

Percentage of total 75 15 9 0.2 0.004


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immunoglobulin in serum(approx)

Serum concentration(mg/dL) (approx)

1000 200 120 3 0.05

Sedimentation coefficient 7S 7S or 11S

1

19S 7S 8SMolecular weight (x1000) 150 170 or 4001 900 180 190

Structure Monomer Monomeror dimer

Monomer orpentamer

Monomer Monomer

H chain symbol E

Complement fixation + +

Transplacental passage +

Mediation of allergicresponses

+

Found in secretions +

Opsonization +

Antigen receptor on Bcell

+ ?

Polymeric form containsJ chain

+ +

Table 62 1 Comparison of Class I and Class II MHC Proteins

Feature Class I MHC

Proteins

Class II MHC

Proteins

Present antigen to CD4-positive cells No Yes

Present antigen to CD8-positive cells Yes No

Found on surface of all nucleated cells Yes No

Found on surface of "professional" antigen-

presenting cells, such as dendritic cells,macrophages, and B cells

Yes1 Yes

Encoded by genes in the HLA locus Yes Yes

Expression of genes is codominant Yes Yes

Multiple alleles at each gene locus Yes Yes

Composed of two peptides encoded in the HLA locus No Yes


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Composed of one peptide encoded in the HLA locusand a -beta2-microglobulin

Yes No

Table 64 2 ABO Blood Groups

Group Antigen on Red Cell Antibody in Plasma

A A Anti-B

B B Anti-A

AB A and B No anti-A or anti-B

O No A or B Anti-A and anti-B

Table 64 3 Compatibility of Blood Transfusions between ABO Blood Groups1

Recipient

Donor O A B AB

O Yes Yes Yes Yes

A (AA or AO) No Yes No Yes

B (BB or BO) No No Yes Yes

AB No No No Yes

Table 64 4 Rh Status and Hemolytic Disease of the Newborn

Rh Status

Father Mother Child Hemolysis

+ + + or No

+ + No (1st child)

Yes (2nd child and subsequent children)

+ No


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+ + or No

No

Table 66 2 Microbial Infections Associated with Autoimmune Diseases

Microbe Autoimmune Disease

1. Bacteria

Streptococcus pyogenes Rheumatic fever

Campylobacter jejuni Guillain-Barr syndromeEscherichia coli Primary biliary cirrhosis

Chlamydia trachomatis Reiter's syndrome

Shigella species Reiter's syndrome

Yersinia enterocolitica Reactive arthritis

Borrelia burgdorferi Lyme arthritis

2. Viruses

Hepatitis B virus Multiple sclerosis

Hepatitis C virus Mixed cryoglobulinemiaMeasles virus Allergic encephalitis

Coxsackie virus B3 Myocarditis

Coxsackie virus B4 Type 1 diabetes mellitus

Cytomegalovirus Scleroderma

Human T-cell leukemia virus HTLV-associated myelopathy

Table 7-1. Cytokines and Their Actions

Cytokine Major Cell Source Major Immunologic Action

IL-1 (, ) MacrophagesEndothelial cellsDendritic cellsLangerhans' cells

Stimulates IL-2 receptor emergence in TcellsEnhances B-cell activationInduces fever, acute phase reactants, andIL-6


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Increases nonspecific resistanceInhibited by an endogenous IL-1receptor antagonist

IL-2 TH1 cells T-cell growth factorActivates NK and B cells

IL-3 T cells Stimulates hematopoiesisIL-4 T cells Stimulates B-cell synthesis of IgEDown-regulation of IFN-

IL-5 T cells Stimulates growth and differentiation ofeosinophilsB-cell growth factorEnhances IgA synthesis

IL-6 MonocytesT cellsEndothelial cells

Induces acute phase reactants, fever, andlate B-cell differentiation

IL-7 Bone marrow Stimulates pre B and pre T cells

IL-8 MonocytesEndothelial cellsLymphocytesFibroblasts

Chemotactic factor for neutrophils and Tcells

IL-9 TH cells T-cell mitogenIL-10 TH2 cells Inhibits IFN- synthesis by TH1 cells

Suppresses other cytokine synthesisIL-11 Bone marrow Stimulates hematopoiesis

Enhances acute phase protein synthesisIL-12 Macrophages

B cellsPromotes TH1 differentiation and IFN-synthesisStimulates NK cells and CD8+ T cells tocytolysisActs synergistically with IL-2

IL-13 TH2 cells Inhibits inflammatory cytokines (IL-1,IL-6, IL-8, IL-10, MCP)

IL-15 T cells T-cell mitogenEnhances growth of intestinal epithelium

IL-16 CD8+ T cellsEosinophils

Increases class II MHC, chemotaxis, andCD4+ T-cell cytokinesDecreases antigen-induced proliferation

IL-17 T cells Increases the inflammatory responseIL-18 Activated

macrophagesIncreases IFN- production and NK cellaction

TNF- MacrophagesT cellsB cellsLarge granularlymphocytes

Cytotoxic for tumorsCauses cachexiaMediates bacterial shock

TNF- T cells Cytotoxic for tumors


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Transforming growthfactor

Almost all normal celltypes

Inhibits proliferation of both T and BcellsReduces cytokine receptorsPotent chemotactic agent for leukocytesMediates inflammation and tissue repair

IFN = interferon; Ig = immunoglobulin; IL = interleukin; MCP = macrophagechemotactic protein; MHC = major histocompatibility complex; NK = natural killer;TNF = tumor necrosis factor.

Acid/base compensationThe mnemonic ROME means the following:

Respiratory Opposite

pH elevated PCO2 diminished = respiratory alkalosis pH diminished PCO2 elevated = respiratory acidosis

Metabolic Equal

pH elevated HCO3 elevated = metabolic alkalosis pH diminished HCO3 diminished = metabolic acidosis

Normal Values and Acceptable Ranges of the ABG Elements

pH 7.4 RangeRange7.35to7.45Pa02

7.35 to 7.45Pa02

90mmHg

Range

80 to

100mmHgSa02

Ran

93 to100%PaC0

2

40mmHg

Range

35 to45mmHgHC0

3

24mEq/L

Range

22 to26mEq/L


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ge

Number One!

Determine if the client is demonstratingan acidotic (remember: pH less than7.35) or alkalotic (pH greater than 7.45).

Number Two!

What is the 'primary problem'

If the client is acidotic with a PaC02greater than 45 mmHg it isRESPIRATORY

If the client is acidotic with a HC03 lessthan 22 mEq/L it is METABOLIC!

If the client is alkalotic with a PaC02less than 35 mmHg it isRESPIRATORY!

If the client is alkalotic with a HC03greater than 26 mEq/L it isMETABOLIC!

Number Three!

Is the client compensating?

Are both components (HCO3 andPaCO2) shifting in the same direction?Up or down the continuum? Above orbelow the normal ranges? If this isnoted, you know that the client sbuffering systems are functioning andare trying to bring the acid-base balanceback to normal.

Uncompensated

pH abnormal (high or low)


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One component abnormal (high or lowCO2 or HCO3)The other component is normal(The component not causing the acid-base imbalance is still normal

Partly compensatedpH not normal (but moving towardnormal)Both CO2 and HCO3 are outside normalrangeThe component that was normal ischanging in order to compensate

Compensated

pH normal

Other values abnormal in oppositedirectionsOne is acidotic the other alkaline

Case Studies :: Case Study 1

A client recovering from surgeryin the post-anesthesia care unit(PACU) is difficult to arouse twohours following surgery. The

nurse in the PACU has beenadministering Morphine Sulfateintravenously to the client forcomplaints of post-surgical pain.The client s respiratory rate is 7per minute and demonstratesshallow breathing. The patientdoes not respond to any stimuli!


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The nurse assesses the ABCs(remember Airway, Breathing,Circulation!) and obtains ABGsSTAT!

The STAT results come backfrom the laboratory and show:

pH = 7.15Pa C02 = 68 mmHgHC03 = 22 mEq/L

Once you have interpreted theABG results, click on one of thefollowing

o Compensated RespiratoryAcidosisUncompensatedMetabolic AcidosisCompensated MetabolicAlkalosisUncompensatedRespiratory Acidosisans


An infant, three weeksold, is admitted to theEmergency Room. Themother reports that theinfant has been irritable,difficult to breastfeed andhas had diarrhea for thepast 4 days. The infant srespiratory rate iselevated and the fontanels

are sunken. TheEmergency Roomphysician orders ABGsafter assessing the ABCs.

The results from theABGs come back from


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the laboratory and show:

pH = 7.37Pa C02 = 29mmHgHC03 = 17mEq/L

Once you haveinterpreted the ABGresults, click on one ofthe following

CompensatedRespiratoryAlkalosisUncompensatedMetabolicAcidosisCompensatedMetabolicAcidosis ansUncompensatedRespiratoryAcidosis


A client, 5 days post-abdominal surgery, has a nasogastric tube. The nursenotes that the nasogastric tube (NGT) is draining a large amount (900 cc in

2hours) of coffee ground secretions. The client is not oriented to person, place,or time. The nurse contacts the attending physician and STAT ABGs areordered.

The results from the ABGs come back from the laboratory and show:

pH = 7.52Pa C02 = 35 mmHg


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HC03 = 29 mEq/L

Once you have interpreted the ABG results, click on one of the followingCompensated Respiratory Alkalosis

Uncompensated Metabolic AcidosisCompensated Metabolic AcidosisUncompensated Metabolic Alkalosis ans


A client is admitted to the hospital and is being prepared for a craniotomy(brain surgery). The client is very anxious and scared of the impending surgery.He begins to hyperventilate and becomes very dizzy. The client loosesconsciousness and the STAT ABGs reveal:



Once you have interpreted the ABG results, click on one of the following

Compensated Metabolic AcidosisUncompensated Metabolic AcidosisUncompensated Respiratory Alkalosis ans

Uncompensated Respiratory AcidosisCase Studies :: Case Study 5

A two-year-old is admitted to the hospital with a diagnosis of asthma andrespiratory distress syndrome. The father of the infant reports to the nurse that hehas observed slight tremors and behavioral changes in his child over the past threedays. The attending physician orders routine ABGs following an assessment ofthe ABCs. The ABG results are:



Once you have interpreted the ABG results, click on one of the followingCompensated Respiratory AlkalosisUncompensated Metabolic Acidosis


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Compensated Respiratory Acidosis ansUncompensated Respiratory Alkalosis

Documents

FCPS Part1 Q BANK~Physiology Flash Cards~Very Important for Part 1