test #26 4.14 Flashcards
how is Ca2+ cleared from cells during relaxationi muscle cells
(1) Ca2+ ATPase on SR
(2) Na+ / Ca2+ exchanger on sarcolemma (3Na in, 1 Ca out)
calmodulin activates some plasma membrane Ca2+ ATPase
how is Ca2+ released from sarcoplasmic reticulum in cardiac myoctes? skeletal?
cardiac: Ca2+ dependent calcium release via ryanodine receptors
skeletal muscle: DHP-tethering of ryanodine receptor (mechanical)
gestational diabetes on fetus
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
rationalization
immature ego defense: invents logical reasons to explain actions actually performed for other reasons (usu to avoid self-blame)
social learning
theory of personality development that emphasizes the important of observing and imitating the behaviors, attitudes, and emotional reactions of others.
bipolar disorder w/ psychotic features vs. schizoaffective disorder?
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.
bipolar disorder diagnosis
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
diagnosis of a manic episode
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
what drug has been shown to reduce mortality in individuals w/ acute coronary syndrome?
beta-blockers
rate limiting step in catecholamine synthesis?
tyrosine hydroxylase (tyrosine –> DOPA (dihydroxyphenylalanine).
bretylium, guanethidine
inhibits vesicular fusion of catecholamines.
iliopsoas, rectus femoris, and tensor fascia lata are impt for..
hip flexion
gluteus maximus, semitendinous, semimembranous, biceps femoris - long head impt for..
hip extension
gluteus medius and minimus impt for
hip abduction
adductor brevis, longus, and magnus impt for..
adduction
how to the ureters gain access to the pelvis? what structures is it between?
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)
what does coagulase in staph do?
reacts w/ prothrombin, converts fibrinogen to fibrin. fibrin-coating of organism makes it resistant to phagocytosis.
toxin released by clostridium perfingers
alpha toxin, lecithinase, phospholipase C degrades phospholipids
inheritance of chronic granulomatous disease
X-linked recessive
phases of acute tubular necrosis
(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
genetics of early onset alzheimer’s (3)? late onset (1)? protective?
early onset:
- APP, chr. 21
- presenilin 1, chr. 14
- presenilin 2, chr. 1
late onset:
-apoE4, chr. 19
protective:
- apoE2, chr 19
genetics of familial hypercholesterolemia (IIa)
autosomal dominant. mutation in LDL receptor – absent or defective.
HET: cholesterol = 300
HOM: cholesterol = 700 (RARE)
increased cholesterol deposits & atherosclerosis
genetics of hyperchylomicronemia (I)
autosomal recessive. mutation in (1) lipoprotein lipase OR (2) apolipoprotein CII.
increased xanthoma but not atherosclerosis.
genetics of hypertriglyceridemia (IV)
autosomal dominant. hepatic overproduction of VLDL. causes pancreatitis.
what is the primary drive respiratory drive? in COPD patients?
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.
why must supplemental oxygen be used with caution in COPD patients?
hypoxemia is now primary respiratory drive. supplemental oxygen HALTS drive.
(bc chronic hypercapnia no longer stimulates respiratory centers)
Hering-Breuer reflexes
pulmonary stretch receptors (myelinated & unmyelinated C fibers in lung & airways)
regulate duration of inspiration/expiration depending on degree of lung distension.
UTI w/ dysuria and hematuria that resolves in a few days most likely caused by…
adenovirus (serotypes 11 and 21 subgroup B)
most common cause of fatal diarrhea in children
rotavirus (a reovirus). often in winter months
sympathetic innervation to the eye pathway (3 order neurons)
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
horners + brachial plexus problems
pancoast lung tumor invasion of superior cervical ganglion and brachial plexus
‘permissive’ effect of hormone
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
tachyphylaxis drug effect
decreased drug responsiveness w/ repeated adinistration
additive drug
combined effect of two drugs = sum of individual drug effects
synergistic:
combined effect exceeds sum of individual drug effects
requires that each drug has some independent effect
cortisol’s effects on BP
permissive. cortisol itself does NOT increase BP.
instead, increases alpha-1 adrenergic receptor expression on vasculature, such that catecholamines (NE) can increase NP
cortisol effects on body
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
when does poststreptococcal glomerulonephritis begin after strep throat/skin infxn? what types
2-4 weeks. type 1, 4, 12
what causes hypercellular glomeruli in acute post-streptococcal glomerulonephritis?
leukocyte infiltration, proliferation of endothelial cells, and mesangial cells
benign familial hematuria
autosomal dominant. thinning of glomerular basement membrane. normal renal fxn. no edema, proteinuria, azotemia.
oval fat bodies in urine?
nephrotic syndrome! hyperlipidemia from increased liver synthetic fxn (due to loss of albumin in urine)
burr cells, or echinocytes?
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
causes of burr cells (echinocytes) vs. spur cells (acanthocytes)
echinocytes: artifact, uremia, pyruvate kinase deficiency, microangiopathic hemoyltic anemia, mechanical damage
acanthocytes: liver disease, abetalipoproteinemia
what is the primary energy source after 24 hours of fasting?
gluconeogenesis!
when do glycogen stores deplete?
12-18 hours of fasting
gluconeogenesis starting substrates (3)
lactate, glycerol, glucogenic amino acids
3 (of the 10) unidirectional enzymes in glycolysis
hexokinase, PFK, and pyruvate kinase (PEP–>pyruvate)
what 4 enzymes in gluconeogenesis overcome irreversible steps of glycolysis?
(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)
pantothenic acid
B5 – acetyl-CoA. needed for many acetylation rxns.
CoA (B5) is important for
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.
presentation of B5 deficiency
very rare. no acetyl-CoA.
paraesthesia and dysesthesias (burning feet syndrome) and GI distress
what explains the rapid recovery from thiopental & other related lipid soluble barbituates?
accumulation in brain is followed by rapid redistribution into skeletal muscles & adipose tissue (within 5 to 10 min).
pralidoxime
cholinesterase enzyme reactivator (good to treat organophosphate poisoning, along with atropine)
drugs that induce hyperkalemia?
(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
hyperkalemia-inducing diuretics in patients w/ renal insufficiency (4)
amiloride, triamterene, spironolactone, epeleperone
high arteriovenous concentration gradient of an inhaled anesthetic suggests
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.
inhaled anesthetics with low peripheral tissue solubility
small arteriovenous gradients, less peripheral tissue uptake. blood saturation occurs quickly. brain concentration equilibrate faster
arteriovenous concentration gradient influences what paramater
RATE of induction. NOT anesthetic potency.
what determines speed of induction / recovery time on inhaled anesthetic?
low blood solubility
what determines potency of inhaled anesthetic
high lipid solubility
minimal alveolar concentration that prevents movement in 50% of patients exposed to noxious stimuli.
potent = LOW mac.
pharmacokinetic properties of N2O
low blood solubility. low lipid solubility. fast induction, low potency.
pharmacokinetic properties of halothane
high blood solubility, high lipid solubility. slow induction, high potency.
DDAVP (desmopressin acetate) can be used in 2 hematological disorders
releases vWF and factor VIII from endothelial cells
von willebrand disease and mild hemophilia A
anaplasia
lack of differentiation
atrophy
decrease in organ size from a reduction in clel size or number
white non-scrapable lesion in mouth of SMOKER?
leukoplakia. precancerous lesion.
white lesion in mouth of immunosuppressed (HIV)
scrapable: candida (oral thrush)
nonscrapable: hairy leukoplakia (EBV)
winters formula
PaCO2 = [ (1.5 x HCO3-) + 8 ] +/- 2
if PaCO2 > than predicted; concurrent respiratory acidosis
PaCO2 < predicted; concurrent respiratory alkalosis
kussmaul respirations
hypernea to blow off CO2
PRP (polyribose-ribitol-phosphate) capsule
H. influenza type B
why are conjugate vaccines (polyssacharide capsule + toxoid) impt in kids?
hard to mount immune response against T-lymphocyte-INDEPENDENT-antigen. toxoid –> increases immunogenicity
how is solubility achieved in vaccine preparations
aluminum hydroxide and aluminum sulfate (protein, i.e. toxoid in conjugate vaccine, impairs solubility)
deficiency of enzymes responsible for porphyrin synthesis (porphyria) can be broadly categorized..
hepatic or erythropoetic (depending on site of enzymatic deficiency)
which 2 places is heme synthesized?
LIVER (cytochrome p450 system)
BONE MARROW (for hemoglobin)
regulated differently. serve different functions
what can induce acute attacks of intermittent hepatic porphyria
phenobarbital, griseofulvin, phenytoin, alcohol, low caloric restriction.
(low hepatic heme, increased ALAS activity, increased d-ALA and porphobillinogen –> acute abdominal pain, neuro symptoms)
sudden onset of focal numbness and tingling that fully resolved within minutes? rx?
TIA
rx? low dose aspirin
(could be seizure, migraine, anxiety, hypoglycemia)
low dose aspirin primarily inhibits? high dose?
LOW DOSE, inhibits cox-1
HIGH DOSE, inhibits cox-1 and 2
differential expression of prostaglandins in platelets & vascular endothelial cells
both express COX 1 and 2.
both process PGH2.
platelet –> thromboxane A2
vascular endothelial –> prostacylcin
thromboxane A2 (platelets) vs. prostacyclin (vascular endothelium)
thromboxane A2: platelet aggregation, vasoconstriction, proliferation of vascular smooth muscle cells
prostacyclin: inhibit aggregation, vasodilation, and inhibit smooth muscle proliferation
how is aspirin induced GI bleeding cause (2)
(1) inhibition of thromboxane A2-mediated platelet aggregation
(2) impaired PGE2 and PGI2 dependent protection of gastrointestinal mucosa
samter’s triad (10% of asthmatics treated with aspirin)
(1) asthma,
(2) aspirin hypersensitivity (nasal symptoms, bronchospasm, facial flushing)
(3) nasal polyposis
due to overproduction of leukotrienes (when COX is blocked).
salicylism (high dose aspirin)
vertigo, tinnitus, hearing loss.
also stimulates respiratory drive –> respiratory alkalosis & salicylate accumulation –> metabolic acidosis
worst headache of life. presentation
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)
berry aneurysms associated with
marfans, ADPCKD, ehleros
bartonella henselae can cause what in immunocompetent vs. immunocompromised individuals
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
potential complication after subarachnoid hemorrhage
vasospasm due to blood breakdown, rx: NIMODIPINE
etoposide and teniposide block
topo II (side = 2) . solid tumors, leukemia, lymphoma
irinotecan, topotecan block
topo I (1 can!) colon cancer, ovarian & small cell lung cancer
what 2 things needed for osteoclast maturation. what inhibits maturation
ALL form osteoblast:
stimulate: MCSF and RANK-L
inhibit: OPG (decoy receptor for RANK)
note: PTH stimulates osteoblasts to increase osteoclast maturation.
VEGF in bone stimualted by
low estrogen
hyperthyroidism vs. pheo?
panic attack vs. pheo?
pheo = usu episodic! (unclear why)
panic attack = usu younger, and isolated systolic increase.
pheo = combined systolic and diastolic.
anticonvulsant (absence, myoclonic, tonic-clonic) and mood stabilizer
valproic acid
- increase Na+ inactivation
- inhibit GABA transaminase
warfarin metabolism
liver P450 system (altered by inducers & inhibitors!)
esp P450 2C9
splenic sequestration crisis
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
progression of spleen in sickle cell
first splenomegaly due to increased splenic destruction of sickled RBCS —-> infarction etc —> splenic atrophy and asplenia
macrocytic anemia in sickle cell patient due to..
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)
3 phases of wound healing
(1) inflammatory (2) proliferative (3) remodeling
- inflammatory - neutrophils & macrophages
- proliferative - granulation tissue & wound contracture
- remodeling - replace type 3 w/ type 1 collagen
role of metalloproteases in wound healing
degradation of collagen & proteins, encourages myofibroblast accumulation at the wound edges and scar tissue remodeling.
wound contraction vs. wound contracture
stimulated by MMPs, myofibroblasts.
excessive –> wound contraction, physical deformity –> skin constriction and functional limitation. due to excess MMP –> excess myofibroblast
wound dehiscence
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
wound ulceration
due to poor vascularization (i.e lower limb injury w/ atherosclerotic peripheral vascular disease)
keloid
hypertrophic scar, excessive collagenous scar tissue deposited by fibroblasts. extends beyond margin of wound.
