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Week 5 Lectures Flashcards

1
Q

Describe clinical features of high body temperature, including infectious/non-infectious etiology and common patterns

A

Remittent fever- elevated T and diurnal fluctuation ex) sepsis, TB
Intermittent fever- episodes of fever separated by days of normal temp ex) malaria
Relapsing fever- fevers every 5-7 days ex) Borreliosis and Colorado Tick fever
Episodic fever- few days then remission for 2 weeks ex) familial periodic fevers
Pel-Ebstein fever- cyclical pattern ex) Hodgkin Lymphoma
Continuous fever- stays elevated for days ex) Typhoid

Etiology- fever can be infectious or non infectious; autoimmune (acute rhematic fever) or endocrine (thyroid storm, pheochromocytoma)

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2
Q

Why is high body temperature deleterious for cell membranes and enzyme activity?

A

enzyme activity is dependent on Temp and pH, hight temperature can denature the enzyme

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3
Q

What is the role of TRPVR1 and CMR1 in neural control of body temperature?

A

TRPVR1- heat receptor 30-46 C
CMR1- cold and menthol receptor 10-24 C

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4
Q

What is the blood-brain barrier (BBB)?

A

endothelial tight junctions, blood vessels that vascularize the CNS

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5
Q

How do circumventricular organs help bypass the BBB for core temperature sensing and cytokine access to the hypothalamic thermostat?

A

permit hormones to leave the brain w/o disrupting BBB. anything in the blood can touch the neurons in OVLT for thermoregulation. binds somatostatin, angiotensin II, and atrial natriuretics

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6
Q

What are the thermoregulation effector organs and their regulators? (hint: glomus bodies, sweat glands, shivering thermogenesis in muscle and non-shivering thermogenesis in liver and, brown adipose tissue, thyroid hormones)

A

Efferents:
Skin arterioles and sweat glands: constrict and dilate vessels
Liver: heat generation (non shivering)
Brown fat: heat generating, uncouplers (nonshivering)
Muscles: shivering

T3 increases expression of Na+K+ATPase and UCP

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7
Q

What is role of ATP generation and ATP hydrolysis via Na+K+-ATPase and SERCA in thermogenesis?

A

Malignant hyperthermia: when there’s ryanodine receptor mutation + Halothane + Succinylcholine –> release of Ca2+ from SR, Inc SR Ca2+ ATPase (SERCA) –> Inc ATP hydrolysis, some E lost as heat, malignant hypothermia

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8
Q

Does fever play a protective role in infection/inflammation?

A

yes, it will kill invading germs before immune response

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9
Q

What are endogenous pyrogens?

A

molecules that can induce fever
interleukin 1-a (IL-1a)
interleukin 6 (IL-6)
tumor necrosis factor- alpha (TNF-a)
interferon- gamma (INF-y)

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10
Q

What are endogenous antipyretics?

A

molecules that prevent fever
glucocoritcoids
a-MSH
AVP (ADH)
melatonin
IL-10

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11
Q

What are endogenous antipyretics?

A

molecules that prevent fever
glucocorticoids
a-MSH
AVP (ADH)
melatonin
IL-10

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12
Q

How does signaling by cytokines cAMP in OVLT-Astrocyte-PON neurons control set point temperature?

A

endogenous pyrogens bind to OVLT endothelial receptors –> hypothalamic endothelial COX 2 ACTIVATION –> Inc PGE2 –> PGE2 binding to EP3 receptor (PTGER3) on Astrocytes –> Dec cAMP and (-) of warmth sensitive neurons –> Inc in Temp –> fever

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13
Q

How does the signaling by cytokines, PGE2 control the set point temperature?

A

Macrophages, lymphocytes, and endothelial cells produce pyrogenic cytokines (IL-1,IL-6, TNF-a), pyrogens induve synthesis of PGE2, Inc PGE2 in periphery leads to myaligas and athraligias
Inc PGE2 in hypothalamus –> fever

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14
Q

How does the difference between fever as raised set point and hyperthermia as heat overload relate to their treatment?

A

because fever is raised set point, it can be treated with NSAIDs, but because hyperthermia involves overwhelming the cooling system and does NOT involve increasing set point, it can only be treated by cooling

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15
Q

Why NSAIDs cannot be used to treat hyperthermia?

A

NSAIDs work by inhibiting COX2 (leads to inc set point), but hyperthermia DOES NOT involve Inc in set point, so only cooling works

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16
Q

What is the best non-specific treatment of hyperthermia? (hint: cooling)

A

cooling blankets, apply ice packs to groin, axilla and neck, spray patient with alcohol and water and cool with fans

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17
Q

idiopathic pulmonary arterial hypertension (PAH_ PGI2 analogs

A

EPOPROSTENOL, TREPROSTINIL, ILOPROST

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18
Q

child with congenital cyanotic heart disease being prepared for surgery: PGE1 analog to maintain temporary patency of ductus arteriosus

A

ALPROSTADIL

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19
Q

child with PDA, COX1/2 inhibitor to close DA

A

INDOMETHACIN

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20
Q

aspirin-induced GI ulcers: methyl PGE1

A

MISOPROSTOL

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21
Q

ripen cervix during labor: PGE2 analog intravaginal gel

A

DINOPROSTONE

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22
Q

Postpartum hemorrhage: methyl PGE1 contracts uterus

A

MISOPROSTOL

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23
Q

Glaucoma: PGF2a analog

A

LATANOPROST

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24
Q

second trimester abortion/postpartum hemorrhage: PGE2a analog

A

CARBOPROST

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25
Q

post-MORPHINE postoperative pain

A

KETOROLAC/ ACETAMINOPHEN IV

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26
Q

osteoarthritis: COX 2 blocker

A

CELECOXIB

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27
Q

fever: COX 1/2 blocker

A

IBUPROFEN

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28
Q

Migraine: COX 1/2 blocker

A

NAPROXEN

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29
Q

Myocardial infarction: COX 1/2 blocker (anti-aggregant effect)

A

ASPIRIN

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30
Q

NOT used to treat asthma as it’s a COX 1/2 blocker and WORSENS bronchoconstriction

A

ASPIRIN

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31
Q

peak age 6-8 year, aspirin use –> triad of fatty liver degeneration, INC ALT and AST, encephalopathy
pathogenesis- hepatocyte mitochondrial dysfunction –> INC NH3 –> encephalopathy
clinical features (1-5 types) 5- fixed dilated pupils –> death (case fatality rate: 25%-50%)
diagnostic- 3 fold inc in ALT/AST and in serum NH3
pathology: no inflammation in liver or brain

A

Reye Syndrome

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32
Q

heat-related exposure (prolonged vs exertional), core temperature > 40 C (104 F), CNS Symptoms (headache, N/V, weakness, confusion, dizziness, delirium, convulsions), skin hot, hyperventilation, multiorgan failure

A

Heat Stroke

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33
Q

prolonged exposure (heat waves, older adults and infants/toddlers), exertional exposure (job, leisure, etc; younger and healthier), predisposing chronic disease, medications, poor nutrition or obesity

A

Heat Stroke

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34
Q

Heat dissipating mechansism; hypothalmic thermoreceptors (preoptic nucleus) –> 1) vasodilation –> convection loss, conduction loss (ineffective when enviroment temp > skin temp) and radtiation loss (blocked w/ high ambient temps) 2) sweating –> evaporation loss (blocked with high humidity) Heat Generation (ambient temp, humidity, activity level) higher than heat disapasstion (impaired mechanism) IL-1 and IL-2 –> multiorgan failure in severe hyperthermia

A

Heat Stroke

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35
Q

prolonged heat exposure- classical (heat waves, high humidity, etc), exertional (sports, labor, military), nausea, vomiting, and thirst; painful muscle craps (myalgias), headache, confusion, convulsions and collapse, organ failure (renal, liver, musculoskeletal, cardiovascular)

A

Heat stroke

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36
Q

core body temp > 40 C (104F), tachycardia, tachypnea, hypotension, agitation, emotional instability, delirium, not alert or oriented, camatose, dry mucous membranes, muscoskeletal (rhabdomyolsis- muscle edema and pain on palation)

A

Heat stroke

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37
Q

clinical diagnosis, core temp > 40C (104F), CNS dysfunction, exposure to heat

ABCs (intubation if needed, intravaneous normal saline), core body temp measurement, foley cather for urine output, manage organ dysfunction, avoid antipyretics (Tylenol); cooling (goal is core temp 39C), ice bath, avoid shivering

A

Heat stroke

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38
Q

acute ingestion, chronic ingestion, tinnitus, vertigo, nausea, vomiting, diarrhea, hyperventilation, respiratory alkalosis, anion gap metabolic acidosis, severe ingestion –> organ disease

acute ingestion- (young, psychiatric history, previous overdose, ingestion history or pill bottles); chronic intoxication (elderly, salicylate’s parts of therapeutic medications, inadverent excessive intake, cared for multiple physicains

A

Aspirin Toxicity

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39
Q

salicylate- directly stimulates medulla, uncomples oxidative phosphorylation, compenatory increase in catabolism (inc O2 consumption, inc heat production, glucose and glycogen depletion, inc CO2), accumulation of organic acids (lactic acid), worsening neurotoxicity as pH dec and crosses into brain tissue

A

Aspirin toxicity

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40
Q

acute ingestion (vomiting, tinnitus, vertigo, lethargy, seizure, coma, CNS/CV collapse), chronic ingestion (elderly adults, prescription meds with ASA, confusion)

acute ingestion- hyperpnea, hyperthermia, decreased alertness; chronic ingestion- signs of dehydration, decreased alertness and orientation; both can lead to crackles on lung exam (edema)

A

aspirin toxicity

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41
Q

arterial blood gas- respiratory alkalosis, metabolic acidosis; salicylate level- monitor levels due to delayed absorption; anion gap w/ metabolic acidosis

ABCs, IV sodium bicarbonate, activated charcoal, urinary alkalinization, hemodialysis

A

Aspirin toxicity

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42
Q

suicide or accidental ingestion, common in children, more severe in adults, early: asymptomatic/mild GI upset followed by liver damage 1-2 days, late: severe hepatic dysfunction and necrosis, elevated APAP level

A

Acetaminophen (APAP) Toxicity

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43
Q

most common cause of acute liver failure, numerous containing medications, Phase 1 (<24h) absorption and metabolism, phase II (24-72 h) liver abnormalities and dysfn, phase III (72-96h) peak liver dysfn, phase IV (4d-2 weeks) recovery, ESLD, or death

A

Acetaminophen (APAP) Toxicity

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44
Q

APAP metabolized safely by glucuronidation and sulfation, ~10% metabolized by CYP-450 –> NAPQI; glutathione assists in conversion to non-toxic metaboline BUT glutathione depleted allows –> toxic metabolites; hepatocyte death w/ centrilobular necrosis

A

Acetaminophen (APAP) Toxicity

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45
Q

suicide attempts, Phase 1- asymtomatic, or nausea and vomiting; Phase II- abdominal pain, jaundice; Phase III- worsening pain and jaundice, bleeding and bruising, encephalopathy; Phase IV- worsening symptoms, improving symptoms

sceral icterus and jaundice, hepatomegaly RUQ tenderness, bleeding and ecchymosis, hypotension and hyperpnea

A

Acetaminophen (APAP) Toxicity

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46
Q

Serum APAP level- timing of ingestion, ideally 4 hours later; liver assessment; BUN, creatine, glucose, electrolytes for anion gap

activated charcoal, N-acetylcysteine (NAC) inc glutathione, binds NAPQI, enhances coagulation; treat anyway if: evidence hepatocytoxicity, detectable level with unkown time, can’t check APAP level

A

Acetaminophen (APAP) Toxicity

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47
Q

intermittent flushing, pruritis (itching), abdominal pain, upper GI tract disease (gastritis, PUD), lower GI tract disease (diarrhea), tachycardia and hypotension (leads to cardiovascular collapse)

slight male predominance, occur at any age, rare, cutaneous form (children), systemic form (adults)

A

Mastocytosis

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48
Q

aspartate to valine substitution of KIT, KIT encodes a stem cell factor receptor, somatic gain of function mutation that is ligand independent, clonal mast cell proliferation, mast cells distrubuted in GI tract

A

Mastocytosis

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49
Q

cardiovascular (weak, fatigue, palpitation), lung (wheezing), gastrointestinal- upper (dyspepsia, cramps, PUD, gastritis,) lower- (diarrhea, pain, cramps); skin (flushing, itching, rash)

cardiovascular- hypotension, tachycardia; lung- wheexing, GI- abdominal tenderness, hepatomegaly and portal hypertension; skin- red-brown macular or papular rash

A

Mastocytosis

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50
Q

Tryptase level, KIT mutation testing, cutaneous biopsy, bone marrow biopsy

H1 and H2 antihistamine, mast cell stabalizer (cromolyn), leukotriene or prostoglandin inhibitors (montelukastat or ASA), epinephrine pen, specific tyrosine/multikinase inhibitors or other cytoreductive therapy

A

Mastocytosis

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51
Q

younger age at onset, episodic subcutaneous and submucosal non-pruritic edema (angioedema), episodic self limited recurrent abdominal pain, no hives or urticaria, may have triggers and mistaken for anaphylaxis

autosomal dominant, rare, first attack typically <15 years old

A

Hereditary Angioedema

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52
Q

deficiency of C1 inhibitor, bradykinin builds up and is the biological mediator of edema, no mast cell activation

A

Hereditary Angioedema

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53
Q

complaints of swelling of parts of body no itching, hoarsness, abdominal pain, prodromal symptoms of rash, tingling, fatigue, accused of “drug seeking”

presence of angioedema, asymmetric swelling, stridor, drooling if severe airway involvement, abdominal pain to palpation

A

Hereditary Angioedema

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54
Q

Check C4 level, without C1 inhibitor, complement of cascade is activated and consumed, C1 inhibitor function

not histamine mediated so epinephrine and steroid have no effect, ABC’s and supportive care, C1 inhibitor, blocade of bradkinin receptor or disruption of kallikrein pathway

A

Hereditary Angioedema

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55
Q

What are endogenous pyrogens?

A

molecules that can induce fever
interleukin 1-a (IL-1a)
interleukin 6 (IL-6)
tumor necrosis factor- alpha (TNF-a)
interferon- gamma (INF-y)

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56
Q

What are endogenous antipyretics?

A

molecules that prevent fever
glucocorticoids
a-MSH
AVP (ADH)
melatonin
IL-10

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57
Q

What are the routes of elimination of drugs?

A

EXCRETION (primarily renal, hepatic, lungs, sweat glands, mammary glands, placenta)
METABOLISM (hepatic)

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58
Q

What is the first-order kinetics of elimination? Which drugs follow this kinetics?

A

amount of drug eliminated is proportional to the amount of drug present in the body (natural decay process)
most drugs follow first order kinetics

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59
Q

What is drug clearance?

A

volume of plasma cleared of a drug in unit time,
determines dose per unit time required to maintains a Cp

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60
Q

Can you calculate elimination rate constant (k) from volume of distribution (Vd), administered I.V. dose (D), and clearance (CL)?

A

k= CL/ Vd
Cp= D/ Vd

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61
Q

What’s the formula for renal clearance of a drug? What values do you need to do this? (hint: Cp, Curine, urine output)

A

CL (mL/min) = urine flow (mL/min) X drug conc. in urine (mg/ML) / Cp (mg/mL)

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62
Q

What’s the formula for half-life of drugs with first order kinetics of elimination?

A

t1/2= 0.7 X Vd / CL

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63
Q

What is zero-order kinetics of elimination? List some drugs that follow this kinetics.

A

decline in Cp (elimination) is constant with time
PHENYTOIN, ETHANOL, ASPIRIN (PEA)

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64
Q

How do you recognize zero and first order kinetics from graphical representation of Cp over time?

A

Zero order: Cp, mg/L (y axis)
First oder: Ln (Cp) (y axis)

65
Q

When can the zero order and first order kinetics graphs look similar in appearance? (hint: look at Y axis)

A

both have downward straight line when zero order y-axis is Cp and first order y-axis is Ln(Cp)

66
Q

What is the relationship between steady-state and half-life?

A

half life determine time to steady state

67
Q

What is bioavailability? How is that calculated from the Cp graphs of oral and IV administration?

A

fraction (F) of an orally administered dose that reaches system circulation, affected by variations in enzyme activity of gut wall or liver, in gastric pH or intestinal motility
always = 1 in IV

F= AUC oral / AUC IV

68
Q

How do you calculate loading dose (LD) and maintenance dose (MD)? In an obese patient?

A

LD= Cp X Vd / F

MD= Cp X CL / F

DOUBLE THE VD for obese patient

69
Q

How does renal function affect dosing?

A

may have to adjust based on renal clearance

70
Q

Which anti-inflammatory drugs block PLA2?

A

GLUCOCORTICOIDS

71
Q

What is the role of PLA2 and PGH synthases in the production of eicosanoids?

A

PLAs- enzyme coverts membrane phospholipid to arachidonic acid

PGH Synthases (bifunctional enzyme COX and HOX)- enzyme converts arachidonic acid to PGH2

72
Q

Which cells and which COX make TxA2 and PGI2?

A

TxA2- TPa-b (platelets, VSMC, kidney, macrophages) COX 1

PGI2- IP- (* endothelium platelets*, kidney, brain) COX 2

73
Q

Which prostaglandin is a platelet aggregate? Which one has antiaggregant action?

A

Thromboxane (TxA2)

Prostacyclin (PGI2)

74
Q

Which tissues express COX-1, 2 & 3?

A

COX 1- ALL CELLS

COX 2- neurons and thick ascending loop cells

COX 3- in CNS

75
Q

What are the physiologic effects of products of the arachidonate cascade on major organs/ tissues (vascular, respiratory, kidney, platelet, uterus, stomach etc.)?

A

PGE2 causes inflammation, redness, heat, pain, and swelling
Leukotrine B4- chemotaxis
Leukotriene C4, D4, E4- bronchospasm, vasoconstriction
Lipoxin A4, B4,- antiinflammatory

76
Q

What is the role of eicosanoids in inflammation, pain, thermoregulation, platelet aggregation, and bronchoconstriction?

A

PGE2 causes inflammation, redness, heat, pain, and swelling
TxA2- platelet aggregation and bronchoconstriction

77
Q

What do the products of 5-LOX do? (hint: chemoattractant LTB4 and bronchoconstrictors LTC4, LTD4 and LTE4)

A

1) Leukotriene B4- chemotaxis (draws neutrophils to site of inflammation)
2) Leukotriene C4, D4, E4- bronchospasm, vasoconstriction
3) Lipoxin A4, B4- antiinflammatory HETs

78
Q

Why is aspirin an irreversible COX inhibitor and how is this property used for prophylaxis of thrombosis? Why is a low-dose (81 mg baby aspirin) used for this?

A

aspirin IRREVERSIBLY acetylates serine/ PGH synthase to decrease TxA2 and inhibit platelet aggregation

platelets exposed to baby aspirin cannot make anymore and achieve anti-aggregation effect

79
Q

Know the side effects of aspirin: salicylism and Reye syndrome

A

salicylism- chronic toxicity, tinnitus (rining in ears), decrease hearing, vertigo

Reye syndrome- fatty liver, inc ALT and AST, encephalopathy due to hepatic mitochondrial dysfunction and Inc NH3

80
Q

Why do the COX-2 inhibitors lack the GI bleeding side effect of non-selective inhibitors? Why do they cause MI?

A

Inhibiting COX 2 only blocks vasodilation, COX 2 in endothelial cells are suppressed by drug CELCOXIB (unwanted affect), TXAs (vasoconstrictor) NOT suppressed so it will cause coronary vasoconstriction –> MI

81
Q

What is the MOA and mechanism of hepatotoxicity of acetaminophen? How to Rx it? (hint: NAC)

A

causes ROS toxicity by consuming all the GSH needed to break down H2O2 to water

N-ACETYLCYSTEINE takes the role of GSH and allows some GSH to be saved for the cells

82
Q

What are the four major effects of NSAIDs?

A

analgesic (relive pain)
anti-inflammatory
anti-aggregant
antipyretic (reduce fever)

83
Q

What do GLUCOCORTICOIDS inhibit

A

PLA2

84
Q

Why do NSAIDs exacerbate asthma?

A

ASPIRIN is a COX1/2 inhibitor and WORSENS bronchoconstriction

85
Q

what drug inhibit COX I and 2

A

NSAIDs (ASPIRIN)

86
Q

what drugs inhibit COX III

A

ACETAMINOPHEN

87
Q

What drug is a COX II selective inhibitor

A

CELCOXIB (no GI bleed)

88
Q

What drug inhibits 5-Lipoxygenase for asthma

A

ZILETUON

89
Q

What drugs are Leukotriene receptor blockers for asthma?

A

MONTELUKAST, ZAFRILUKAST, PRANLUKAST

90
Q

Why is the parasympathetic NS called craniosacral? Where are the locations of preganglionic neurons?

A

because it innervates CN 3,7,9,10 and S2-S4

91
Q

Why is the sympathetic NS called thoracolumbar? Where are the locations of preganglionic neurons?

A

intermediolateral (IML) gray matter of the spinal cord at the level of T1-L2

92
Q

What is the role of autonomic NS in homeostasis?

A

respiration, digestion, circulation, metabolism, etc

93
Q

What are the anatomical units and their location of the sympathetic and parasympathetic NS?

A

somatic (sensory and motor)- voluntary
autonomic (sensory and motor)- involuntary
Sympathetic- spinal cord IML T1-L2
Parasympathetic- CN 3,7,9,10 and IML S2-S4

94
Q

What is the difference between pre- and paravertebral ganglia?

A

paravertebral (“beside the vertebrae”) ganglia are called the sympathetic chain ganglia
Prevertebral ganglia- located around the major branches of the abdominal aorta and include the celiac, aortic renal, superior mesenteric, and inferior mesenteric ganglia

95
Q

What are the similarities and differences in the structure and function of sympathetic and parasympathetic NS?

A

both in autonomic nervous system, sympathetic- fight or flight, parasympathetic- rest and digest

96
Q

Why is the parasympathetic NS called craniosacral? Where are the locations of preganglionic neurons? (hint: cranial nerve (III, VII, IX, X) and sacral (S2-S4) origins of the parasympathetic NS)

A
97
Q

What are the receptor subtypes associated with the autonomic NS in major organs?

A

a1, a2, b1, b2

98
Q

Which neurotransmitters are released by the pre- and postganglionic neurons of the sympathetic NS?

A

pre- ACh
post- norepinephrine and epinephrine

99
Q

Which neurotransmitters are released by the pre- and postganglionic neurons of the parasympathetic NS?

A

ACh

100
Q

What is special about innervation of sweat glands? Which ANS innervates it? What is released by the postganglionic neuron of the sympathetic NS at the sweat gland?

A

sweat glands use ACh (instead of NE) as a postganglionic neuron which is parasympathetic BUT sweating is a sympathetic response

101
Q

Which ANS receptors mediate vasoconstriction and vasodilation?

A

a1- vasoconstriction
a2- vasodilation

102
Q

What are the steps in acetylcholine and norepinephrine synthesis and degradation?

A
103
Q

Where are the cholinergic and adrenergic receptors distributed?

A

vascular SMC, sweat glands, heart, etc

104
Q

What are the physiological effects of cholinergic and adrenergic agonism in major organs?

A

Cholinergic agonist- stim ACH –> parasympathetic response
Adrenergic agonist- lower bp and heart rate

105
Q

Explain why succinylcholine, being a cholinomimetic by action, actually causes paralysis of skeletal muscles

A

succinylcholine adheres to post-synaptic cholinergic receptors of the motor endplate, inducing continuous disruption that results in transient fasciculations or involuntary muscle contractions and subsequent skeletal muscle paralysis.

106
Q

Explain how pralidoxime treats poisoning with ACh-esterase inhibitors such as pesticides

A

breaks/reverses covalent bonds formed byorganophosphates

107
Q

Explain how an ACh-esterase inhibitor can protect from nerve gases that are also ACh-esterase inhibitors

A

nerve gases bind covalently to Cys residues on acetylcholinesterase and produce toxic levels of ACh
Temporarily blocking AChE prevents nerve gases from binding

108
Q

Explain the differential effects of NE and Epinephrine on vascular tone, cardiac function and bronchial tone

A

epinephrine affects your heart, norepinephrine affects the blood vessels

109
Q

Explain how a β1 and β2 agonist both acting via Gs GPCR can have opposing effects on muscle contraction/relaxation in different tissues

A

B1- Inc HR, Inc renin secretion (heart and kidneys)
B2- bronchodilation, Inc HR (contraction), (-) insulin secretion, vasodilation

110
Q

Explain why epinephrine but not NE is a good choice to treat anaphylactic shock

A

epinephrine acts on the bronchioles to allow air flow during anaphylactic shock

111
Q

Why an anticholinesterase drug would activate both NN and M3 receptors?

A

both act on sweat glands

112
Q

Which receptors mediate the drug treatment of anaphylaxis? (hint: two of epinephrine receptors)

A

α1 and β2 adrenergic receptors

113
Q

Which receptor mediates the action of Epi in skin blood vessels? In the heart for Rx of systole?

A

a1
B1

114
Q

Which receptor mediates the orthostatic hypotension in BPH treatment?

A

a-1

115
Q

Why NE cannot be used to treat anaphylactic shock?

A

not effective because it’s an agonist for a1, a2, B1 and DOES NOT HAVE B2 AGANOSIM TO DILATE BRONCHI as EPi does

116
Q

What is the rate limiting enzyme in catecholamine biosynthesis?

A

tyrosine hydroxylase (TH)

117
Q

Variable that the experimenter manipulates or changes to observe its effect on other variables

A

independent variable

118
Q

what is affected by independent variable

A

dependent variable

119
Q

measuring the association btw a risk factor and a disease

A

quantifying risk

120
Q

used to compare individuals with and without a disease based on exposure to a risk factor (2x2 table)

A

contingency table

121
Q

measure of association btw an exposure and an outcome, represents the odds of exposure among cases vs odds of exposure among controls

A

odd ratio (OR)

122
Q

measure of risk of a certain event happening in an individual of one (exposed) group to risk of the same event happening to an individual in another (unexposed group)

A

relative risk

123
Q

if RR = 1 means there is ___ association between exposure and disease

A

no

124
Q

if RR > 1, exposure associated with ____ disease occurrence.
if RR < 1, exposure associated with ____ disease occurrence.

A

increased
decreased

125
Q

tells you by how much the treatment reduced the risk of bad outcomes relative to the control group who did not have the treatment, %

A

relative risk reduction (RRR)

126
Q

difference in risk btw exposed and unexposed

A

attributable risk (AR)

127
Q

difference in risk (not the proportion) attributable to the intervention compared to the group, actual difference

A

absolute risk reduction (ARR)

128
Q

number of patients needed to be treated for 1 patient to benefit

A

number needed to treat (NNT)

129
Q

number of patients who needed to be exposed to a risk factor for 1 patient to be harmed

A

number needed to harm (NNH)

130
Q

% of deaths occuring among those with disease

A

case fatality rate (CFR%)

131
Q

number of deaths in a defined population over a defined period

A

mortality rate

132
Q

proportion of exposed people who become ill

A

attack rate

133
Q

proportion of the incidence of a disease in the population (both exposed and unexposed) due to exposure
ex) low birth weight due to prenatal smoking

A

population attributable risk (PAR)

134
Q

percent of the incidence of a diease in the population (both exposed and unexposed) that is due to the exposure

A

population attributable risk %

135
Q

occurence of new cases of disease or injury in a population over a specified period of time, NEW CASES

A

incidence

136
Q

number of cases of a disease in a specific population at a specified time or over a specified period of time, EXISTING cases

A

prevalence

137
Q

OR = 1 means odds of exposure are ____ in cases and controls

A

equal

138
Q

OR > 1 means odds of exposure are greater among _____

A

cases

139
Q

OR < 1 means odds of exposures are greater in _____

A

controls

140
Q

number of patients who need to be treated for 1 patient to benefit

A

number needed to treat (NNT)

NNT = 1/ ARR
ideal NNT is 1

141
Q

number of patients need to be exposed to a risk factor for 1 patient to be harmed

A

number needed to harm (NHH)

NNH= 1/ AR
higher number = safer exposure

142
Q

mathematical framework for analyzing random phenomenon

A

probability thery

143
Q

mathematical tool used to study randomness and provide predictions about how likely something is to happen

A

probabiltiy

144
Q

tells you how likely a patient has a disease or condition, higher the ratio the more likely the patient has disease

A

likelihood ratios (LR)

145
Q

probability of one event occuring with some relationship

A

conditional probability

146
Q

mathematical formula for determining conditional probabilty

A

Bayes’ Theorem

P (A/B) = P (B/A) X P(A) / P(B)

147
Q

probability of having disease before a diagnostic test is performed

A

pre-test probability

P (D+) = (true positive + false negatives) / total

148
Q

probability of having disease after a diagnostic test is performed

A

post-test probabilty

149
Q

screening tests ability to correctly identify individuals with a disease as positive for that disease

A

sensitivity (true positive)

sensitivity = true positive / true positive + false negative

150
Q

screening tests ability to correctly identify individuals who do not have a disease as negative

A

specificity (true negative)

151
Q

probability that a person who has a positive test result actually has the disease

A

positive predictive value

152
Q

probability that a person who has a negative test result who does not actually have the disease

A

negative predicitive value

153
Q

purpose is to detect asymptomatic and early stage disease ex) mammograms

A

screening

154
Q

degree to which the test actually measures what it claims to measure; “accuracy”

A

validity

155
Q

degree to which a test is consistent and reproducible in measuring what is is intended to measure, “precision”

A

reliability

156
Q

used to depict the tradeoff btw test sensitivity and specificity and choose an appropriate test threshold, greater area under curve indicated greater test usefulness

A

ROC curves

157
Q

a hypothesis is chosen and the subsequent research focuses on answering that hypothesis (causation)

A

hypothesis driven

158
Q

researcher searches data for patterns and relationships (causation)

A

hypothesis generating

159
Q

a group of principles that provide limited support for establishing evidence of a casual relationship between presumed cause and effect
temporality* and dose response*

A

Bradford Hill Criteria

PFM (5 decks)

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