High Yield Notes Flashcards

heart rate
Terms Definitions
Inhibits dihydrofolate reductase
Plasmid-mediated resistance
TMP/SMX has synergetic effect from the sequential blockade of folate synthesis since SMX blocks dihydropterate synthase, which is an exzyme that converts paraaminobenzoic acid into dihydrofolate
Produces a disulfiram-like reaction
Treatment of esophageal candidiasis in AIDS
Cholinomimetic used in treating open angle glaucoma
Inotropic (increase contractility) vasodilator (decreases afterload) that activates alpha and Beta1>Beta2 activity without much chronotropic effect
Used in the treatment of shock (cardiogenic) associated with hypotension and hypotension associated with renal failure or CHF
Stimulates Cardiac Beta1 receptors, peripheral alpha-receptors, and dopaminergic receptors in vessels in the renal and splanchnic bed
At low doses, it is primarily a vasodilator that increases renal and splanchnic blood flow
At high doses, it increases cardiac contractility (inotropic) and cardiac output via its activation of cardiac Beta1 receptors
Via its own receptors in the thalmus, limbic structures, and cerebral cortex which are part of the GABA receptor-chloride ion channel macromolecular complex, benzodiazepines facilitate the inhibitory action of GABA via increased conductance in the chloride ion channel
Flumazenil blocks this effect by blocking the receptor for benzodiazepines and is the treatment of choice for benzodiazepam overdose
An elderly woman on thiazides is most at risk for developing?
A child who ingests 30 adult aspirins will most likely develop
An increased anion gap metabolic acidosis
Children, unlike adults, do not commonly develop a mixed metabolic acidosis and respiratory alkalosis
Rx is to perform gastric lavage and add activated charcoal and to produce an alkaline urine for increased excretion of the acid
Open angle glaucoma is best treated with
Beta1 and Beta2 blockers
Timolol is a favored agent
Pilocarpine may also be used
Open angle glaucoma is the MC type of glaucoma: produces gradulal loss of peripheral vision (tunnel vision) and optic atrophy
Second generation anti-depressant
inhibition of serotonin reuptake
May cause priapism
Retinitis pigmentosum may be a complication
Weak estrogen that acts as an antagonist in breast tissue (estrogen competes with tamoxifen for binding to the receptor) and partial agonist in uterus (can produce endometrial hyperplasia)
Also protects against osteoporosis and can be used in women who have ERA positive tumors
Can be used in treating progestin-resistant endometrial cancer
Complications: Flushing (menopausal symptoms), vaginal bleeding, potential for endometrial hyperplasia/cancer
Analgesic and antipyretic but not an anti-inflammatory agent
Inhibits prostaglandin synthesis in the CNS
Very weak cyclooxygenase inhibitor
MC drug causing acute fulminant hepatitis
Converted into free radicals in the liver
Glutathione inactivates the FRs
Acetylcysteine treatment replaces GSH
Digitalis toxicity
Treat with digifab
First generation: drug of choice for surgical prophylaxis in many cases
Second generation: Rx of sinusitis (cefuroxime); Rx of mixed anaerobic infections
Third generation: Rx of meningitis; Rx of GC and Lyme's disease (ceftriaxone)
Blocks D4 (dopamine) and 5-HT3 receptors moreso than D2
Fever in a patient on a loop diuretic:
Do not use any type of NSAID since it blocks renal synthesis of prostaglandin, which vasodilates the afferent arteriole
Use acetaminophen to lower fever, since it does not interfere with protaglandin synthesis
Loop diuretics lead to volume depletion, hence angiotensin II will be elevated (vasoconstricts efferent arteriole); loss of prostaglandin effect predisposes the patient to renal failure
Red man syndrome
IV vancomycin
Drug for bacterial carrier states (S. aureus, N. meningitidis, H. influenzae)
Single dose drug for GC and Chlamydia
Rx of malignant hypertension
Antihypertensive and antiarrhythmic drug that lowers blood pressure and increases heart rate:
Lipid effects: lowers LDL/VLDL
Prevents osteoporosis: inhibits osteoclast activating factor (IL-1) secreted by osteoblasts
Thrombogenic: natural estrogens are less thrombogenic than synthetic estrogens; increase synthesis of coagulation factor; decrease ATIII;
Increases liver synthesis of transcortin and thyroid binding globulin: increases total cortisol/thyroxine levels without an increase in free hormone
Increases liver synthesis of sex hormone (testosterone or androgen) binding globulin: lowers free testosterone
Cancer risk: endometrial, breast, intrahepatic cholestasis, cholelithiasis
Analgesic and antipyretic but not an anit-inflammatory agent
Inhibits prostaglandin synthesis in the CNS
Very weak cyclooxygenase inhibitor
MC drug causing acute fulminant hepatitis
Converted into free radicals in the liver- glutathione inactivates the FRs, acetylcysteine treatment replaces GSH
Digitalis toxicity:
Treat with digoxin antibodies (FAB fragments)
Oral contraceptives:
Pill effects: Inhibits LH surge, which prevents ovulation
Increase malar eminence pigmentation: "pregnancy mask"
Ethinyl estradiol (synthetic estrogen) increases liver synthesis of many proteins
19-norestrosterone (progestational agent) effects: Water retention/weight gain, reduction in estrogen receptor synthesis (atrophy of endometrial glands), increase LDL, decrease HDL
Complications: thrombogenic, stimulate trypptophan metabolism; lowers serotonin - depression, increases liver synthesis of angiotensinogen: MCC of HTN in young women, intrahepatic cholestasis, hepatic adenoma: tendency to rupture, increasegallstone formation
Cancer risks: cervical, breast controversial, hepatocellular carcinoma
Protective pill effects: fibrocystic change in teh breast, endometrial cancer, ovarian cancer: less ovulation reduces risk for cancer: pelvic inlammatory disease: Neisseria gonorrhoeae not Chlamydia trachomatis; uterine leiomyomas, endometriosis, acne, rheumatoid arthritis, hirsutism
Iron toxicity:
Clinical setting: accidental overdose of ferrous sulfate in children
S/S of iron toxicity: hemorrhagic gastritis, hepatic necrosis wiht liver failure, shock/metabolic acidosis, x-rays reveal undigested radiopaque pills in GI tract
Rx- iron binding agents, oral phosphate or bicarbonate salts (precipitate unabsorbed iron), parenteral deferoxamine
Organophhosphate poisoning:
MOA: irreversible block of acetylcholine esterase (noncompetitive inhibitor), accumulation of acetylcholine at synapses/myoneural junctions
Source: pesticides,
Initial autonomic system overactivity: excessive lacrimation/salivation, fecal incontinence, constricted pupils
Nicotinic effects later in toxicity: muscle weakness and paralysis, muscle fasciculations, low serum and RBC cholinesterase (pseudocholinesterase)
Rx: atroopine Rx of choice, pralidoxime (2-PRAM) also may be used
Rx of HTN
Weight reduction is the most important factor in lowering BP
Carbonic anhydrase inhibitors:
MOA: blocks the proximal reclamation of bicarbonate
Bicarbonate binds iwth Na ions and is excreted in teh urine (diuretic effect)
Produces a normal AG metabolic acidosis form bicarbonate lost in the urine
Clinical uses:
Chronic management of glaucoma: reduces the rate of aqueous humor formation and reduces intraocular pressure
Alkalinizes the urine: good Rx for drug toxicities 9salicylate intoxication)
Rx of acute mountain sickness: produces metabolic acidosis, which is the compensation for respiratory alkalosis
Clinical uses of thiazides
Initial drug used in Rx of HTN in elderly patients: also reduces the incidence of strokes and fatal AMIs in tehis age group
Initial drug used in Rx of systolic HTN in the elderly
One of the initial drugs used in Rx of HTN in African Americans
Rx of choice in treatment of nephrogenic diabetes insipidus: volume depletion from increased proximal reabsorption of NA and water reduces degree of polyuria
Rx of hypercalciuria in calcium stone formers
Rx of proximal RTA: increases reclamation of bicarbonate
Clinical uses of loop diuretics:
Initial drug used in Rx of HTN in chronic renal failure
Rx of choice for hypercalcemia after a diuresis is started with isotonic saline
CHF with acute pulmonary edema
Rx of halide poisonings: fluoride, bromide
Acute renal failure: flush out tubular cells obstructing the lumen and can change an oliguric to polyuric renal failure
MOA of spironolactone:
Blocks the aldosterone-enhanced Na/K pump in the late distal convoluted tubule and collecting duct: K sparing effect, danger of hyperkalcemia
Blocks the proton/K pump in the collecting tubules: danger of normal AG metabolic acidosis
Blocks androgen receptors: Rx of hirsutism, produces gynecomastia in men
MOA of triamterene/amiloride:
They are not aldosterone inhibitors, they block Na reabsorption and the secretion of K in the aldosterone -enhanced Na/K pump: K sparing effect
MOA of non-selective Beta blockers
Block Beta receptors in teh heart: reduce sympathetic stimulation, reduce BP, decreased contractility of the heart, decrease heart rate, reduce secretion of renin in kidneys
Block Beta recetors in teh smooth muxcle and liver: blocks catecholamine-induced glycogenolysis
MOA of selective Beta1 blockers
Cardioselective beta blockers
Primarily target Beta 1 receptors in the heart
Less bronchoconstriciton than nonselective blockers
Side effects of Beta blockers
Conduction disturbances: AV block, block adrenergic signs/sx ofinsulin/oral sulfonylurea-induced hypoglycemia in diabetes mellitus- does not block sweating
Incude bronchospasm in those with asthma- less bronchoconstriction with selective types
Lipid effects (mainly in non-selective)
Increase TG decrease HDL
Rebound angina
Hypertension if abruptly withdrawn- up regulation of Beta adrenergic receptors occurs when they are blocked
Clinical uses of Beta-blockers:
Congestive heart failure and acute myocardial infarction- increases survival
Cardiac arrhythmias
Essential tremor- benign condition with trembling of hands
Prevention of migraine headaches
Graves' disease- blocks adrenergic signs and symptoms
Hypertrophic subaortic stenosis
MOA of alpha-adrenergic blockers:
In lowering BP, they block post-synaptic alpha-adrenergic receptors
Vasodilate arterioles/venules
Reduce vascular resistance
Relax smooth muscle in urinary bladder and prostate: useful in Rx of BPH
Unlike Beta-adrenergic blockers, they lower TG and CH, and increase HDL
Nonselective types block alpha1 and alpha2 adrenergic blockers- produce too much compensatory tuypes of effects (tachycardia
Side-effects of alpha-adrenergic blockers
Dizziness due to orthostatic hypotension
Prazosin may produce a positive serum ANA
Alpha-Adrenergic blockers phenoxybenzamine and phentolamine:
Produces a chemical sympathectomy
Rx of hypertensive episodes wiht pheochromocytoma until surgical removal of tumor
Phentolamine- Rx of hypertensive episodes due to pheochromocytoma during surgery
Rx of skin necrosis and ischemia in accidental inections of epinephrine or other vasoconstricotrs
MOA of clonidine:
Centrally acting adrenergic drugs: examples include clonidine, methyldopa
Stimulate alpha2 adrenergic receptors and imidazoline receptors in the CNS
Reduces efferent peripheral sympathetic outflow
Reduction in blood pressure due to reduction in cardiac output: decreased heart rate and vasodilation of resistance vessels
Increase renal blood flow
MOA of methyldopa: same as for clonidine, converted by central nonadrenergic neurons into methylnorepinephrine, it's active metabolite
Side-effects for methyldopa: Coombs positive hemolytic anemia, Drug induced SLE, drug induced hepatitis: may be fulminant
MOA of calcium channel blockers:
Examples: Verapamil, diltazem, nimodipine, nicardipine
block L-type calcium channels in smooth muscle and cardiac muscle
Peripheral arteriole vasodilator: no venular dilatation
Decrease cardiac contractility and heart rate: negative inotropic and chronotropic effece, respectively
coronary artery vasodilatation
MOA of hydralazine, minoxidil, nitroprusside
Arteriolar vasodilator: hydralazine and minoxidil
Arteriolar/venular dilatator: nitroprusside
No effect on reducing left ventricular muscle mass
Side effects: drug induced SLE with a positive serum ANA: hydralazine, minoxidil: hypertrichosis
Nitroprusside: thiocyanate toxicity
Initial drugs used in Rx of hypertension (HTN) in African-Americans:
Calcium channel blockers: addded if the desired goal is not established
ACE inhibitors or AT II-receptor blockers
Initial drug used in Rx of HTN in DM:
Ace inhibitors are the Rx of choice: HTN control is the single most important factor in preventing a loss of renal function in DM
Initial drug used in Rx of HTN in CHF:
ACE inhibitors are the Rx of choice
Drugs used in Rx of HTN in pregnancy
Methyldopa hydralazine- alternative drug choice
Drug used in Rx of HTN in a patient with urinary retention form prostate hyperplasia:
Alpha-Adrenergic blocker
drugs used in Rx of HTN in asthmatics:
Initial drug used in Rx of HTN in a patient iwth osteoporosis:
Thiazides- increased calcium reabsorption in the kidneys
ACE inhibitor
Decreases preload-inhibit aldosterone
Decreases afterload-inhibit AT II
Hydralazine, minoxidill:
Decrease afterload alone- vasodilators
Decreases preload: venodilator
Decreases afterload: vasodilator
Rx of choice in treatment of malignant hypertension and lowering blood pressure in a dissecting aortic aneurysm
Decreases preload alone: reduces volume by losing salt and water
Decreases afterload alone: vasodilator
An antioxidant that is used in treating recurrent xanthelasmas
May produce torsade de pointes (polymorphic ventricular tachycardia), lowers HDL levels
Nicotinic acid and fibric acid derivatives:
Capillary lipoprotein lipase
Hence increasing the hydrolysis of VLDL in the circulation
HMG CoA reductase inhibitors and fibric acid derivatives
Should not be used together since they both may be associated wiht rhabdomyolysis and the potential for polyuric acute renal failure
HMG CoA reductase inhibitors, nicotinic acid, and fibric acid derivatives:
Associated with drug-induced hepatitis wiht elevation of the transaminases
HMG CoA reductase inhibitors and bile acid resins:
Upregulate LDL receptors synthesis on hepatocytes, hence lowering scrum CH and LDL
HMG CoA reductase in hibitors and nicotinic acid
Inhibit enzymes in tehir mechanisms of action of lowering lipids
Flushing associated wiht nicotinic acid:
Controlled pretreatment wiht aspirin
Fibric acid derivatives:
Greatest overall effect of all lipid lowering agents in raising HDL levels
HMG CoA reductase inhibitor and fibric acid derivatives:
Increase the chance for warfarin toxicity
Bile acid resins:
Lower warfarin levels, hence causing undercoagulation of patients on warfarin
Bile acid derivatives:
Cause a malassimilation of drugs that are commony used in teh treatment of heart disease
Nicotinic acid:
Drug of choice for familial combined hypercholesterolemia and in owering Lp (a)
HMG CoA reductase inhibitors:
Drugs of choice for lowering LDL
Nicotinic acid and fibric acid derivatives:
Significant effect in lowering triglyceride levels
lowers LDL levels
INcrease bone density
Fibric acid derivatives:
Associated with the inappopriate ADH syndrome
Types of drugs of abuse (DOA):
Sedatives: barbiturates, alcohol,
Stimulants: cocaine
Hallucinogens:lysergic acid diethylamide
MC Drugs of abuse in adolescents
CNS effects of long-term drug abuse:
Damage to neurotransmitter receptor sites
Drug screening
Urine best screening medium for DOA
Blood also used in drug assays
Sympathomimetic drug of abuse syndrome:
Examples: amphetamines, cocaine
S/S: tachycardia/sweating, mydriasis (pupil dilation), hypertension, hyperthermia
Anticholinergic drug of abuse syndrome:
Examples: antidepressant, antihistamines, antiparkinson-type medications, atropine, muscle relaxants
S/S: mydriasis, fever, dry skin
Opiate/sedative drug uf abuse syndrome
Heroin, benzodiazepines, barbiturates
S/S: respiratory depression leading to respiratory acidosis, miotic pupils (pinpoint), hypotension
Psychedelic/hallucinogenic drug of abuse syndrome
Antidotes used in unconscious patients:
Dextrose: R/O possible hypoglycemia from insulin overdose
Naloxone: possible opiate overdose
IV thiamine: glucose may precipitate Wernicke's encephalopathy in alchoholics wiht thiamine deficiency
IV drug abuse MC
Localized infection in skin abscess due to Staphylococcus aureus
HBV MC systemic infection
Infective endocarditis: MC tricuspid and aortic valve
S. aureus MCC
Tetanus: complication of "skin popping"
Derived form poppy plant
Usually "cut" wiht some agene: granulomatous reactions occuring in skin/lungs form the cutting agents
Non-cardiogenic pumnary edema: frotheing form teh mouth is common
Focal segmental glomerulosclerosis: Hypertension + Nephrotic syndrome
Rx: naloxone, a morphine derivative wiht a high affinity for opioid binding sites of the mu receptor type
MC DOA in health professionals
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
By-product of attempted synthesis of meperidine
Produces irreversible parkinson's: cytotoxic to neurons in nigrostriatal dopaminergic pathways
Legal synthetic opioid taken orally: mainly used to detoxify opiate abusers
Long acting drug
Saturates CNS opiate receptors
Prevents suddne euphric action associated with heroin
Causes physical dependence/tolerance
Benzodiazepine toxicity:
MOA: enhance the frequency of opening up of GABAa receptor-chloride ion channels leading to increases chloride ion conductance
GABA is an inhibitory neurotransmitter
Drug of choice for alcohol withdrawal syndrome
Rx of toxicity: flumazenil, an antagonist of benzodiazepine and does not block barbiturates or other depressants
Barbiturate toxicity
MOA: enhance the duration of opening of the GABAa receptor chloride ion channels leading to increases chloride ion conductance
Depress neuronal activity in reticular activating system: inhibits the inhibitory effects of GABA and glycine (an amino acid inhibitory neurotransmitter)
Bulae over pressure points: erythema mutiforme
Alkalinizing the urine increases its excretion and lowers blood concentrations
MCCOD from DOA in US
Blocks uptake of neurotransmitters dopamine/NOR by presynaptic axon
Predisposes to: sudden death, acute MI, stroke, pulmonary edema, ventricular arrhythmias, myocarditis
S/S: hypertension, sinus tachycardia, psychosis, sezure acitvity, mydriasis
MOA: release catecholamines form presynaptic terminals
Examples: amphetamines:
Rx obesity, methylphenidate
Rx ADHD and narcolepsy methamphetamine
Ice is street form of the drug
Hallucinations: drug that most simulates schizophrenia
MC illegal DOA used in USMOA: contains the psychoactive stimulatn THC which binds to receptors in substantia nigra, globus pallidus, hippocampus, cerebellum
Derives from leaves adn flowering tops of hemp plants Cannabis sativa)
Hashish is extractd resin of mariuana that has 5-10 times the potency of the parent compound
High lipid solubility: THC is present in urine for more than a week
clinical uses: cancer: decreases NV in cancer patients,
Lower intraocular pressure in glaucoma
S/S of marijuana use: reddening of conjunctiva, euphoria, delayed reaction time: engineer driving a train involved in a crash with an oncoming train was found to have THC metabolites in his urine
LSD (lysergic acid diethylamide)
MOA: ergot alkaloid that binds to D2 dopamine receptors in the brain
Also blocks 5-HT2 serotonin receptor in peripheral tissue
Predisposes to chromosomal breakage leading to congenital defects
S/S: LSD toxicity: hallucinations, flashbacks,
Angel dust
MOA reacts with opioid-like sigma receptors and subtypes of glutamate receptors (antagonists)
Initially introduced as a dissociative anesthetic: separates bodily functions from the mind without a loss of consciousness
S/S of PCP toxicity: aggitation/violent behavior; coma with eyes open; impervious to pain
Use of Beta-blocker in Rx of Graves disease:
Thyroid hormones normally upregulate synthesis of Beta-receptors that interact with catecholamines and produce many of the symptoms of thyrotoxicosis
Giving Beta-blockers, blocks teh Beta-receptors, hence blocking the adrenergic symptoms of thyrotoxicosis
Electrolyte changes when giving insulin:
Drives glucose into the cell along with potassium and phosphate
Rx of carcinoid syndrome
Ocreotide (somatostatin analogue)
Also used in Rx of acromegaly and ViPomas
Patient went into congestive heart failure. What drug could have potentiated this?
Potent negative tnotropic effect
Patient with asthma not responding to albuterol:
Rx with corticosteroid medihaler
Patient with pneumonia due to a gram positive diplococcus (Strep pheumoniae)
Rx with Penicillin G, which blocks cell wall synthesis
Vasodilator used to Rx impotence
Gingo biloba
Improves memory
Saw Palmetto
Rx prostate hyperplasia
Wound healing
Rx of jet-lag
St. Johns Wort:
Rx of depression
Cosmetic hair growth
Green tea
Antioxidant, decrease cancer
Functions of medullary thick ascending limb`
Generation of free water via the active Na+/K+/Cl- co-transport pump
This pump is the most sensitive part of the nephron for damage due to tissue hypoxia
Blocked by loop diuretics
Pump also reabsorbs calcium (not PTH-enhanced)
Functions of cortical thick ascending limb
Na+/Cl- pump in early distal tubule-
Na+ and Ca++ (PTH enhanced reabsorption) cations share the same channel for reabsorption
Blocked by thiazides
Functions of the macula densa
Interacts with the uxtaglomerular (JG) apparatus on teh afferent arteriole
Increased Na+ in the urine inhibits renin release and vice versa
Functions of aldosterone-enhanced ATPase Na+/K+ exchange pump in distal collecting tubule and collecting ducts:
Na+ is reabsorbed in exchange for K+
Effect of increased distal delivery of Na+ from more proximal acting diuretics (loop diuretic or thiazide diuretic)
There is an augmented Na+/K+ exchange, which may lead to hypokalemia and increased reabsorption of bicarbonate (metabolic alkalosis)
Functions of aldosterone enhanced H+/K+ ATPase pump and H+ ATPase pumps in the alpha-intercalated cells in the collecting ducts
Primary sites for the excretion of excess H+ ions
Dysfunction of the H+/K+ ATPase pump is the primary cause for type I distal RTA
Normal dilution of urine
UOsm in thelate distal collecting tubule/collecting duct is normally ~150 mOsm/kg
Primarily contains free water and a smaller amount of obligated water that must accompany solute
When POsm is low, ADH is inhibited: absence of ADH causes teh loss of free water in the urine
Positive free water clearance: CH2O=V-COsm, where CH2O=free water clearance
V=volume of urine in mL/min
COsm=obligated water
To calculate COsm: COsm=UOsm x V/POsm
A positive CH2O indicated dilution (free water is lost in the urine)
Example: urine volume 10mL
POsm 250 mOsm
UOsm 150 mOsm: COsm = 150 x 10/250 = 6mL
CH2O = 10-6 = 4mL
Normal concentration of urine:
Increase in POsm is a stiulus for ADH release
ADH renders the late distal and collecting ducts permeable to free water (not Na+, cannot reabsorb obligated wwater)
Urine is concentrated
Negative CH2O (free water is reabsorbed back into the blood)
Urine volume 10mL
POsm 300 mOsm/kg
UOsm 900 mOsm/kg
COsm=900 x 10/300 = 30mL
CH2O = 10-30 = -20mL
Ability to concentrate urine is the first abnormality in renal failure
Central and nephrogenic DI
Both have low UOsm an dincreased POsm
Central DI shows> 50% increase in UOsm with administration of vasopressin
Nephrogenic DI shows <50% increase in UOsm with vasopressin
Respiration changes with increasing altitude:
Respiratory alkalosis
Hypoxemia due to decreased atmospheric pressure not a decrease in % oxygen in air
Increase in 2,3-BPG right shifts the ODC
Effect of VIP (vasointestinal peptide) and enkephalins on GI tract
VIP relaxes smooth muscle, increases intestinal secretion, increases pancreatic secretion
Enkephalins (opiates) contract smooth muscle, decrease intestinal secretion
Synthesized in Sertoli cells in seminiferous tubules
Negative feedback wiht FSH
Increased if seminiferous tubules are destroyed
Normal if Leydig cells are destroyed, since testosterone has a negative feedback with LH
Hormone increading/decreasing gastric secretions
Hormones inhibiting acid secretion: secretin and gastric inhibitory peptide
Placental anatomy/physiology:
Maternal surface has slightly bulging areas called cotyledons which are covered by a layer of decidua basalis
Fetal surface is entirely covered by the chorionic arteries (venous blood returning form teh fetal heart) adn 1 umbilical vein (carries oxygenated blood from the placenta)
Chorionic villus/umbilical cord, chorionic villi project in the intervillous space, which contains maternal blood from which oxygen is extracted: spiral arteries from the uterus empty into the space
chorionic villi are lined by trophoblastic tissue: outside layer is composed of syncytiotrophoblast: synthesizes hCG and human placental lactogen (growth hormone of pregancy) and inside layer is composed of cytotrophoblast: clear cells, the interior of the chorionic villus has fetal blood vessels, which coalesce to form the chorionic vessels that converge with the umbilical cord
The umbilical cord contains 2 umbilical arteries (contains deoxygenated blood exiting the fetal heart and returning to the placenta) and 1 umbilical vein (contains oxygenated blood)
Effect of increased total peripheral resistance on vascular function curve
Same as teh venous return curve, which depicts the relationship between venous return and right arterial pressure
Increasing TPR (vasoconstriction) decreases venous return to heart, decrease right atrial pressure and decrease ardiac output
This causes a counterclockwise rotation of the curve: venous return increases, right atrial pressure increases, and cardiac output increases
Has luteinizing hormone activity
Keeps corus uteum of pregnancy synthsizing progesterone until 8-10 weeks and then placenta takes over the function
Stimulation of histamine H2 receptors:
Increases secretion of acid by parietal cells
GI peptide injected into cerebrospinal fluid that increases appetite for carbohydrate:
Somatostatin: this normally is made in hypothalamus where is functions to inhibit growth hormone, hence inhibiting GH causes hypoglycemia and the body would crave more carbohydrate to increase glucose levels
Atrial naturiuretic peptide:
mediated by guanylate cyclase, increased if left or right atrium is volume overloaded
Central diabetes insipidus:
Injecting vasopressin causes an increase in urine concentration (POsm) and decrease in urine volume
Location of angiotensin converting enzyme:
Pulmonary capillaries
Increased in sarcoidosis
Non-competitive inhibition by ACE inhibitors
Vitamin D type in kidneys:
Kidney has 1alpha-hydroxylase in proximal tubules (PTH stimulates synthesis)
Renal disease MCC of hypovitaminosis D
Effect of thyroid hormone excess on bone:
Osteoporosis: increases bone turnover resulting in loss of bone mass
Central diabetes insipidus
Injecting vasopressin causes an increase in urine concentration (POsm) and decrease in urine volume
Primary site for temperature regulation:
Anterior hypothalamus
Fever is due to release of pyrogens stimulating IL-1 release from macrophages
IL-1 increases synthesis of PGE2 in the anterior hypothalamus
PGE2 raises the hypothalamic set-point (normal core temperature viewed as too low), nhence anterior hypothalamic reactions of heat generation prevail
Heat generating mechanisms if core temperature is below set-point include:
Increasing the release of thyroid hormones (increases metabolic rate)
Vasoconstriction of skin vessels (sympathetic stimulation of hormones slpha-receptors in smooth muscles)
Sympathetic stimulation of Beta-receptors in brown fat (increases metabolic rate and heat production)
Shivering (most effective system, center located in polsterior hypothalamus, leads to activation of alpha and gamma motoneurons innervating skeletal muscle)
Heat dissipating mechanisms (coordinated in posterior hypothalamus) if core temperature is above set-point include: reducing sympathetic tone (vasodilation) of skin vessels leading to shunting of blood through venous plexus in teh ski
Increased sympathetic activity of cholinergic fibers innervating sweat glands leading to sweating
Cause of decrease in jugular venous pulse on inspiration:
Decrease in lung compliance (sarcoidosis)
Decreased volume of air in the alveoli leads to less copression of vessels in the interstitial tissue, hence they fill up better and drain blood off easier
Iron reabsorption:
Meat has heme iron, which is ferrous and easy to reabsorb in the small intestine (primarily the duodenum):
Once absorbed into enterocytes, heme is enzymatically degraded to release iron,
Most of the iron is diverted to storage as ferritin in the enterocyte (called apoferritin)
While a small amount is delivered to plasma transferrin, the circulating binding protien of iron
Plants have non-heme iron, which is in the ferric state
non-heme iron furst binds to mucin in teh stomach (renders it insoluble)
The mucin-non-heme complex then binds to proteins on the mucosal surface of the duodenum for transport into the cotosol where it is enzymatically degraded to release iron
A cytosolic protein called mobilferrin transfers the iron to the mucosal ferritin stores or to transferrin in the plasma
When body stores of iron are replete, mucosal cells are shed with their stored mucosal ferritin in order to prevent iron overload and tranferrin synthesis in the liver is decreased
When body stores are depleted, most of the iron is directed towards transferrin in the plasma and transferrin synthesis in the liver is increased
Renal reabsorption curve:
Glucose is most often asked aobut
Destory hypothalamus, what hormone increaes:
Prolactin- no dopamine to inhibit
Effect of carotid message:
Slows heart rate
Major site of water reabsorption in the GI tract
In descending order:
Most effective nephron site for acid excretion
Proximal tubule of the kidney
Nephron site for ADH effect
collecting duct
Nephron site for greatest generation of free water/most susceptible to ischemia:
Thick ascending limbin the medulla
constriction of the efferent arteriole:
Increases the GFR and decreases renal plasma flow
filtration fraction in the glomerulus:
constrict afferent arteriole, no change in FF (decrease GFR/decrease RPF)
constrict efferent arteriole increases FF
Increase plasma protein concentration, hence increasing oncotic pressure, decreases the FF
Decreasing plasma proeitn concentration, hence decreasing oncotic pressure, increases the FF
constricting the ureter, decreases PBS, hence decreasing GFR and the FF without affecting RPF
Negative charege of GBM
heparan sulfate
Carotid massage
Decreases heart rate and increases vasodilation (carotid sinus baroreceptor innervated by the IX and Xth nerve
Impulses generated in this receptor inhibit tonic discharge of vasoconstrictor nerves and excite vagal innervation of the heart producing vasodilation, venodilation, drop in blood pressure and heart rate, and a decrease in cardiac output
3% Hypertonic saline and effect on POsm and ADH levels:
3% hypertonic saline increases POsm
Increased POsm stimulates the release of ADH (increases)
Atrial natriuretic peptide is also stimulated and normally does inhibit ADH release, however, hypertonicity overrides ANP
Patient walking briskly on a hot day:
No increase in rectal temperature, vasodilation of vessels in skin
Marathon runner on a hot day:
Increase in rectal temperature
Vasodilation of vessels in skin
Vagus nerve functions in teh stomach
Increases gastric acid secretion and gastric motility: vagotomy decreases acid secretion and motility
The vagus nerve represents the parasympathetic innervation of the stomach and duodenam
Sympathetic nervous system in teh stoach/duodenum:
Inhibits secretion and motility
Sympathetic fibers are located in teh celiac plexus form T5-T9
Hormone modulating GI muscle activity
0.9% normal saine with KCl
The crystalloid solution used to replase gastric loses
Creatinine clearance (CCr)
Creatinine clearance formula: CCr=UV/P
V=24 hour urine (mL/min)
Creatinine is not a perfect clearance substance
Causes of a decreased CCr: increasing age, inadequate 24hr urine collection(decreased urine volume in the numerator), renal failure
Causes of an increased CCr: Normal pregnancy (increase in plasma volume increases GFR and CCr), early diabetic nephropathy
FENa+ (fractional excretion of sodium)
Useful in the workup of oliguria: FENa+=(UNa+ x PCr)/(Pna+ x UCr) x 100
Values<1 indicate intact tubular function
Values >1 (usually >2) indicate tubular dysfunction
Myocardial physiology:
Cardiac hypertrophy increases wall stress, sinus tachycardia reduces filling of the coronary arteries
Increasing heart rate raises myocardial oxygen consumption: cardiac muscle uses Beta-oxidation of fatty acids for energy
Venoconstriction: increases preload alone
Restrict salt and water intake: decreases preload alone
Increase cardiac contractility: no change in preload/afterload
Normal gas physiology at the tissue level:
CO2 derived from tissue enters teh RBC adn combines with H2O via carbonic anhydrase to form H2CO3
H2CO3 dissociates into H+ and HCO3 teh latter leaving the RBC in exchange for Cl- anions
H+ combines with oxygenated Hgb-O2 which releases O2
O2 leaves the RBC, dissolves in plasma an dincreases capillary PO2
Normal gas physiology at the pulmonary level:
Alveolar O2 diffuses into the plasma of the pulmonary capillary owing to a greater partial pressure of alveolar O2
O2 enters the RBC and combines with ferrous ions on deoxyhemoglobin to form oxyHgb and H+
HCO3 enters the RBC from the plasma and combines with H+ to form H2CO3
Cl- anions leave the RBC to counterbalance the entry of HCO3-
H2CO3 dissociates into CO2 and H2O: CO2 leaves the RBC and dissolves in the plasma to increase the PCO2, which enters the alveoli for excretion
Important anatomical considerations for urine control:
Urogenital diaphragm: muscles of the urogenital diaphragm are the deep transverse perineal and sphincter urethra muscle
Location of the UG diaphragm on a cystourethrogram is just distal to the prostate in a male
Location of the urogenital diaphragm on a cystourethrogram in a female is the beginning of urethra where it exists the bladder
Functions of the detrusor muscle: relaxed: storage of urine in the bladder, contracted: emptying of bladder
Functions of the sympathetic in bladder control: relaxes the detrusor muscle: aids in urine storage in teh bladder, contracts internal sphincter: increases urine storage
functions of the parasympathetic system: contracts the detrusor muscle: empties teh bladder, relaxes the internal sphincter muscle by blocking sympathetic inhibition: allows emptying of the bladder
Thyroid hormone
Diffuses into cytosol
Binds to receptors in teh nucleus: DNA binding domain has zinc fingers, other hormones wiht similar binding: steroids, retinoic acid, vitamin D
Synthesized in liver
Increased synthesis form estrogen
Major vehicle for crrying CO2 in blood
Bicarbonate (70%)
Residual volume
volume of air left over after maximal expiration
Total lung capacity
Amount of air in a fully expanded lung, measured wiht a nitrogen or helium dilution method
Functional residual capacity
Total amount of air in the lungs at the end of a normal expiration (end of TV)
Obtained by a helium dilution technique or body plethysmography
Forced vital capacity
Total amount of air expelled after a maximal inspiration: the RV is what is left over at the end of maximal expiration: normal FVC is 5L
Forced Expiratory volume in 1 second
How much air a person can expel from the lungs in 1 second after a maximal inspiration
Normal FEV1 is 4L
Ratio of FEV1/FVC
Normally 0.80: 4/5L
Peak expiratory flow meter: outpatient method of evaluating forced vital capacity (FVC), commonly used by asthmatics to evaluate their airways
Method for measuring RV
Subtract teh expiratory reserve volume (ERV) from the functional residual capacity (FRC)
ERV is the amount of air forcibly expelled at teh end of a normal expiration (end of the TV)
Diffusion capacity (DLco)
DLco is the method of measuring the ability of a gas to diffuse through the alveolar/capillary interface: utilizes CO
DLco is primarily dependent on the following parameters: CO reaching the alveoli (decreased due to V/Q mismatches: atelectasis, COPD),
CO crossing the alveolar/capillary interface (decreased due to pulmonary fibrosis or fluids in the interface)
/ 172

Leave a Comment ({[ getComments().length ]})

Comments ({[ getComments().length ]})


{[ comment.comment ]}

View All {[ getComments().length ]} Comments
Ask a homework question - tutors are online