test #26 4.14 Flashcards Preview

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Flashcards in test #26 4.14 Deck (102)
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1
Q

how is Ca2+ cleared from cells during relaxationi muscle cells

A

(1) Ca2+ ATPase on SR
(2) Na+ / Ca2+ exchanger on sarcolemma (3Na in, 1 Ca out)

calmodulin activates some plasma membrane Ca2+ ATPase

2
Q

how is Ca2+ released from sarcoplasmic reticulum in cardiac myoctes? skeletal?

A

cardiac: Ca2+ dependent calcium release via ryanodine receptors

skeletal muscle: DHP-tethering of ryanodine receptor (mechanical)

3
Q

gestational diabetes on fetus

A

glucose enters baby’s circulation. insulin does not.

high maternal glucose –> hyperglycemia in baby –> causes beta-cell hyperplasia in baby.

post birth, continued increased insulin secretion in baby –> hypoglycemia, and increased fat deposition

4
Q

rationalization

A

immature ego defense: invents logical reasons to explain actions actually performed for other reasons (usu to avoid self-blame)

5
Q

social learning

A

theory of personality development that emphasizes the important of observing and imitating the behaviors, attitudes, and emotional reactions of others.

6
Q

bipolar disorder w/ psychotic features vs. schizoaffective disorder?

A

schizoaffective: schizophrenia + mood symptoms.

at least 2 wk period stable psychotic symptoms (in the absence of prominent mood symptoms)

bipolar disorder: mainly defined by presence of manic episodes.

7
Q

bipolar disorder diagnosis

A

bipolar I: at least 1 manic episode (w/ or w/o hypomanic or depressive episode)

bipolar II: presence of a hypomanic and a depressive episode

8
Q

diagnosis of a manic episode

A

DIG FAST. lasting at least 1 week. requiring hospitalization or 3 of the following

distractibility
irresponsible (seek pleasure w/o regard to consequence)
grandiosity

flight of ideas
activity/agitation
sleep (less)
talkative

9
Q

what drug has been shown to reduce mortality in individuals w/ acute coronary syndrome?

A

beta-blockers

10
Q

rate limiting step in catecholamine synthesis?

A

tyrosine hydroxylase (tyrosine –> DOPA (dihydroxyphenylalanine).

11
Q

bretylium, guanethidine

A

inhibits vesicular fusion of catecholamines.

12
Q

iliopsoas, rectus femoris, and tensor fascia lata are impt for..

A

hip flexion

13
Q

gluteus maximus, semitendinous, semimembranous, biceps femoris - long head impt for..

A

hip extension

14
Q

gluteus medius and minimus impt for

A

hip abduction

15
Q

adductor brevis, longus, and magnus impt for..

A

adduction

16
Q

how to the ureters gain access to the pelvis? what structures is it between?

A

cross OVER common iliac, UNDER gonadal & ovarian vessels.

enters pelvis at bifurcation of iliac (L4)

LATERAL to internal iliac.
MEDIAL to ovarian artery (in women. in men, testicular artery never enters pelvis – just goes to pelvic brim –> inguinal canal)

17
Q

what does coagulase in staph do?

A

reacts w/ prothrombin, converts fibrinogen to fibrin. fibrin-coating of organism makes it resistant to phagocytosis.

18
Q

toxin released by clostridium perfingers

A

alpha toxin, lecithinase, phospholipase C degrades phospholipids

19
Q

inheritance of chronic granulomatous disease

A

X-linked recessive

20
Q

phases of acute tubular necrosis

A

(1) initiation (ischemic / nephrotoxic)
(2) maintenance
- increased fluid retention
serum:
- HIGH: K+, H+, anions (sulfate, phosphate, urate), Mg,
- LOW: Na+, Ca2+

(hypocalcemia due to low vitamin D!)

urine:
HIGH Na (FeNa > 1)
LOW osmolarity

(3) recovery
- vigorous diuresis (high volume hypotonic)
- risk of HYPOKALEMIA –> most worriesome

21
Q

genetics of early onset alzheimer’s (3)? late onset (1)? protective?

A

early onset:

  • APP, chr. 21
  • presenilin 1, chr. 14
  • presenilin 2, chr. 1

late onset:
-apoE4, chr. 19

protective:
- apoE2, chr 19

22
Q

genetics of familial hypercholesterolemia (IIa)

A

autosomal dominant. mutation in LDL receptor – absent or defective.

HET: cholesterol = 300
HOM: cholesterol = 700 (RARE)

increased cholesterol deposits & atherosclerosis

23
Q

genetics of hyperchylomicronemia (I)

A

autosomal recessive. mutation in (1) lipoprotein lipase OR (2) apolipoprotein CII.

increased xanthoma but not atherosclerosis.

24
Q

genetics of hypertriglyceridemia (IV)

A

autosomal dominant. hepatic overproduction of VLDL. causes pancreatitis.

25
Q

what is the primary drive respiratory drive? in COPD patients?

A

increased CO2 (central chemoreceptors)

hypoxemia only kicks in when extreme (PaO2 < 60) in aortic & carotid bodies.

COPD: chronic CO2 no longer stimulates respiratory centers. HYPOXEMIA is primary drive.

26
Q

why must supplemental oxygen be used with caution in COPD patients?

A

hypoxemia is now primary respiratory drive. supplemental oxygen HALTS drive.

(bc chronic hypercapnia no longer stimulates respiratory centers)

27
Q

Hering-Breuer reflexes

A

pulmonary stretch receptors (myelinated & unmyelinated C fibers in lung & airways)

regulate duration of inspiration/expiration depending on degree of lung distension.

28
Q

UTI w/ dysuria and hematuria that resolves in a few days most likely caused by…

A

adenovirus (serotypes 11 and 21 subgroup B)

29
Q

most common cause of fatal diarrhea in children

A

rotavirus (a reovirus). often in winter months

30
Q

sympathetic innervation to the eye pathway (3 order neurons)

A

1st order: posteriorlateral hypothalamus (paraventricular nucleus)

descend down to spinal cord

2nd order: interomediolateral cell column of T1-T2.

3rd order: superior cervical ganglion.

postganglionic fibers travel with internal carotid to eyelid, dilator pupillae, sweat glands, etc

31
Q

horners + brachial plexus problems

A

pancoast lung tumor invasion of superior cervical ganglion and brachial plexus

32
Q

‘permissive’ effect of hormone

A

when hormone allows another hormone to achieve it’s full potential

i.e. NE produces some vasoconstriction. with cortisol, NE produces even MORE. cortisol itself does nothing.

cortisol = permissive; via gene transcription

33
Q

tachyphylaxis drug effect

A

decreased drug responsiveness w/ repeated adinistration

34
Q

additive drug

A

combined effect of two drugs = sum of individual drug effects

35
Q

synergistic:

A

combined effect exceeds sum of individual drug effects

requires that each drug has some independent effect

36
Q

cortisol’s effects on BP

A

permissive. cortisol itself does NOT increase BP.

instead, increases alpha-1 adrenergic receptor expression on vasculature, such that catecholamines (NE) can increase NP

37
Q

cortisol effects on body

A

BIG FIB
big increase, fib decrease

INCREASED:

  • blood pressure (upregulate alpha-1 expression in vessels, such that NE can increase BP more
  • insulin resistance (serine phosphorylation of downstream molecules)
  • gluconeogenesis, lipolysis, proteolysis

DECREASED:

  • low fibroblast activity –> striae
  • low inflammatory & immune response: (inhibit leukotriene, prostaglandin synthesis, inhibit leukocyte adhesion, block histamine release, reduces eosinophils, blocks IL-2 production)
  • low bone formation –> decrease osteoblast activity
38
Q

when does poststreptococcal glomerulonephritis begin after strep throat/skin infxn? what types

A

2-4 weeks. type 1, 4, 12

39
Q

what causes hypercellular glomeruli in acute post-streptococcal glomerulonephritis?

A

leukocyte infiltration, proliferation of endothelial cells, and mesangial cells

40
Q

benign familial hematuria

A

autosomal dominant. thinning of glomerular basement membrane. normal renal fxn. no edema, proteinuria, azotemia.

41
Q

oval fat bodies in urine?

A

nephrotic syndrome! hyperlipidemia from increased liver synthetic fxn (due to loss of albumin in urine)

42
Q

burr cells, or echinocytes?

A

erythrocytes w/ short, evenly spaced projections (smaller & more evenly spaced compared to acanthocytes)

caused by artifact (EDTA), uremia, pyruvate kinase deficiency, microangiopathic hemolytic anemia, mechanical damage

43
Q

causes of burr cells (echinocytes) vs. spur cells (acanthocytes)

A

echinocytes: artifact, uremia, pyruvate kinase deficiency, microangiopathic hemoyltic anemia, mechanical damage
acanthocytes: liver disease, abetalipoproteinemia

44
Q

what is the primary energy source after 24 hours of fasting?

A

gluconeogenesis!

45
Q

when do glycogen stores deplete?

A

12-18 hours of fasting

46
Q

gluconeogenesis starting substrates (3)

A

lactate, glycerol, glucogenic amino acids

47
Q

3 (of the 10) unidirectional enzymes in glycolysis

A

hexokinase, PFK, and pyruvate kinase (PEP–>pyruvate)

48
Q

what 4 enzymes in gluconeogenesis overcome irreversible steps of glycolysis?

A

(1) pyruvate –> oxaloacetate
(pyruvate carboxylase).

(2) oxaloacetate –> PEP
(PEP carboxykinase)

(3) fructose 1,6 bisphosphate –> fructose 6 phosphate
(fructose 1,6 bisphosphotase)

(4) glucose-6-phosphate –> glucose
(glucose-6-phosphatase)

49
Q

pantothenic acid

A

B5 – acetyl-CoA. needed for many acetylation rxns.

50
Q

CoA (B5) is important for

A

acetylation rxns (like first step of TCA), synthesis of vitamin A, D, cholesterol (acetyl-coA –> HMG-CoA reductase), heme A, fatty acids (acetyl-CoA carboxylase) amino acids, proteins.

51
Q

presentation of B5 deficiency

A

very rare. no acetyl-CoA.

paraesthesia and dysesthesias (burning feet syndrome) and GI distress

52
Q

what explains the rapid recovery from thiopental & other related lipid soluble barbituates?

A

accumulation in brain is followed by rapid redistribution into skeletal muscles & adipose tissue (within 5 to 10 min).

53
Q

pralidoxime

A

cholinesterase enzyme reactivator (good to treat organophosphate poisoning, along with atropine)

54
Q

drugs that induce hyperkalemia?

A

(1) nonselective beta blockers (interfere w/ b2-mediated intracellular K+ uptake)
(2) cardiac glycosides (inhibit Na/K ATPase

anything that blocks aldosterone secretion:

(3) ACE inhibitors
(4) ARBs
(5) NSAIDs (reduce local prostaglandin synthesis, reducing renin / aldosterone

55
Q

hyperkalemia-inducing diuretics in patients w/ renal insufficiency (4)

A

amiloride, triamterene, spironolactone, epeleperone

56
Q

high arteriovenous concentration gradient of an inhaled anesthetic suggests

A

high tissue solubility –> more anesthetic must be absorbed to saturate the blood & then the brain.

blood saturation takes longer, so brain saturated is delayed –> onset of action is slower.

57
Q

inhaled anesthetics with low peripheral tissue solubility

A

small arteriovenous gradients, less peripheral tissue uptake. blood saturation occurs quickly. brain concentration equilibrate faster

58
Q

arteriovenous concentration gradient influences what paramater

A

RATE of induction. NOT anesthetic potency.

59
Q

what determines speed of induction / recovery time on inhaled anesthetic?

A

low blood solubility

60
Q

what determines potency of inhaled anesthetic

A

high lipid solubility

minimal alveolar concentration that prevents movement in 50% of patients exposed to noxious stimuli.

potent = LOW mac.

61
Q

pharmacokinetic properties of N2O

A

low blood solubility. low lipid solubility. fast induction, low potency.

62
Q

pharmacokinetic properties of halothane

A

high blood solubility, high lipid solubility. slow induction, high potency.

63
Q

DDAVP (desmopressin acetate) can be used in 2 hematological disorders

A

releases vWF and factor VIII from endothelial cells

von willebrand disease and mild hemophilia A

64
Q

anaplasia

A

lack of differentiation

65
Q

atrophy

A

decrease in organ size from a reduction in clel size or number

66
Q

white non-scrapable lesion in mouth of SMOKER?

A

leukoplakia. precancerous lesion.

67
Q

white lesion in mouth of immunosuppressed (HIV)

A

scrapable: candida (oral thrush)
nonscrapable: hairy leukoplakia (EBV)

68
Q

winters formula

A

PaCO2 = [ (1.5 x HCO3-) + 8 ] +/- 2

if PaCO2 > than predicted; concurrent respiratory acidosis
PaCO2 < predicted; concurrent respiratory alkalosis

69
Q

kussmaul respirations

A

hypernea to blow off CO2

70
Q

PRP (polyribose-ribitol-phosphate) capsule

A

H. influenza type B

71
Q

why are conjugate vaccines (polyssacharide capsule + toxoid) impt in kids?

A

hard to mount immune response against T-lymphocyte-INDEPENDENT-antigen. toxoid –> increases immunogenicity

72
Q

how is solubility achieved in vaccine preparations

A

aluminum hydroxide and aluminum sulfate (protein, i.e. toxoid in conjugate vaccine, impairs solubility)

73
Q

deficiency of enzymes responsible for porphyrin synthesis (porphyria) can be broadly categorized..

A

hepatic or erythropoetic (depending on site of enzymatic deficiency)

74
Q

which 2 places is heme synthesized?

A

LIVER (cytochrome p450 system)

BONE MARROW (for hemoglobin)

regulated differently. serve different functions

75
Q

what can induce acute attacks of intermittent hepatic porphyria

A

phenobarbital, griseofulvin, phenytoin, alcohol, low caloric restriction.

(low hepatic heme, increased ALAS activity, increased d-ALA and porphobillinogen –> acute abdominal pain, neuro symptoms)

76
Q

sudden onset of focal numbness and tingling that fully resolved within minutes? rx?

A

TIA

rx? low dose aspirin

(could be seizure, migraine, anxiety, hypoglycemia)

77
Q

low dose aspirin primarily inhibits? high dose?

A

LOW DOSE, inhibits cox-1

HIGH DOSE, inhibits cox-1 and 2

78
Q

differential expression of prostaglandins in platelets & vascular endothelial cells

A

both express COX 1 and 2.
both process PGH2.
platelet –> thromboxane A2
vascular endothelial –> prostacylcin

79
Q

thromboxane A2 (platelets) vs. prostacyclin (vascular endothelium)

A

thromboxane A2: platelet aggregation, vasoconstriction, proliferation of vascular smooth muscle cells

prostacyclin: inhibit aggregation, vasodilation, and inhibit smooth muscle proliferation

80
Q

how is aspirin induced GI bleeding cause (2)

A

(1) inhibition of thromboxane A2-mediated platelet aggregation
(2) impaired PGE2 and PGI2 dependent protection of gastrointestinal mucosa

81
Q

samter’s triad (10% of asthmatics treated with aspirin)

A

(1) asthma,
(2) aspirin hypersensitivity (nasal symptoms, bronchospasm, facial flushing)
(3) nasal polyposis

due to overproduction of leukotrienes (when COX is blocked).

82
Q

salicylism (high dose aspirin)

A

vertigo, tinnitus, hearing loss.

also stimulates respiratory drive –> respiratory alkalosis & salicylate accumulation –> metabolic acidosis

83
Q

worst headache of life. presentation

A

subarachnoid hemorrhage. abrupt onset. fever, nuchal rigidity, usu no focal neurological deficits.

often from rupture of berry aneursym

blood between arachnoid and pia. CT w/o contrast –> diagnostic. blood / xanthochromia in CSF (yellow CSF)

84
Q

berry aneurysms associated with

A

marfans, ADPCKD, ehleros

85
Q

bartonella henselae can cause what in immunocompetent vs. immunocompromised individuals

A

immunocompetent: cat scratch fever (low fever, lymphadenopathy, self-limited)
immunocompromised: bacillary angiomatosis, red purple papular skin resions. can be found in viscera. fatal if intreated.

also cultured negative endocarditis

86
Q

potential complication after subarachnoid hemorrhage

A

vasospasm due to blood breakdown, rx: NIMODIPINE

87
Q

etoposide and teniposide block

A
topo II (side = 2) . 
solid tumors, leukemia, lymphoma
88
Q

irinotecan, topotecan block

A
topo I (1 can!) 
colon cancer, ovarian & small cell lung cancer
89
Q

what 2 things needed for osteoclast maturation. what inhibits maturation

A

ALL form osteoblast:
stimulate: MCSF and RANK-L

inhibit: OPG (decoy receptor for RANK)
note: PTH stimulates osteoblasts to increase osteoclast maturation.

90
Q

VEGF in bone stimualted by

A

low estrogen

91
Q

hyperthyroidism vs. pheo?

panic attack vs. pheo?

A

pheo = usu episodic! (unclear why)

panic attack = usu younger, and isolated systolic increase.

pheo = combined systolic and diastolic.

92
Q

anticonvulsant (absence, myoclonic, tonic-clonic) and mood stabilizer

A

valproic acid

  1. increase Na+ inactivation
  2. inhibit GABA transaminase
93
Q

warfarin metabolism

A

liver P450 system (altered by inducers & inhibitors!)

esp P450 2C9

94
Q

splenic sequestration crisis

A

young children w/ sickle cell. due to vasocclusion and splenic pooling of blood cells.

medical emergency (10-15% mortality rate). marked decrease in hemoglobin concentration, rapidly enlarging spleen, possible hypovolemic shock.

repeated splenic infarction –> fibrosis and atrophy of spleen

95
Q

progression of spleen in sickle cell

A

first splenomegaly due to increased splenic destruction of sickled RBCS —-> infarction etc —> splenic atrophy and asplenia

96
Q

macrocytic anemia in sickle cell patient due to..

A

folic acid deficiency, due to increased erythrocyte turnover.

impaired DNA synthesis, normal RNA synthesis. cytoplasmic components grow but cells divide slowly –> chubs.

(accelerated erythropoiesis also increases MCV due to reticulocytosis, but not as markedly as folate deficiency would)

97
Q

3 phases of wound healing

A

(1) inflammatory (2) proliferative (3) remodeling

  1. inflammatory - neutrophils & macrophages
  2. proliferative - granulation tissue & wound contracture
  3. remodeling - replace type 3 w/ type 1 collagen
98
Q

role of metalloproteases in wound healing

A

degradation of collagen & proteins, encourages myofibroblast accumulation at the wound edges and scar tissue remodeling.

99
Q

wound contraction vs. wound contracture

A

stimulated by MMPs, myofibroblasts.

excessive –> wound contraction, physical deformity –> skin constriction and functional limitation. due to excess MMP –> excess myofibroblast

100
Q

wound dehiscence

A

rupturing of previously closed wound. result from insufficient granulation & scar tissue formation, inadequate wound contraction, or excessive mechanical stress.

often in abdominal wounds – increased intraabdominal pressure

101
Q

wound ulceration

A

due to poor vascularization (i.e lower limb injury w/ atherosclerotic peripheral vascular disease)

102
Q

keloid

A

hypertrophic scar, excessive collagenous scar tissue deposited by fibroblasts. extends beyond margin of wound.