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Physiology Flashcards

1
Q

MAP

A

(SBP + 2DBP) / 3

CO x Total Peripheral Resistance

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2
Q

CO =

A

SV + HR

rate of O2 consumption / (arterial - venous O2 content)

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3
Q

CO at rest and exercise

A

5 L/min –> 20 L/min

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4
Q

Renal plasma flow

A

RPF estimated by calculating paraaminohippuric acid (PAH) clearance

filtration fraction FF = GFR / RPF

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5
Q

GFR calculation

A

Kf ((Pg-PB) - (piG - piB))

kf = filtration coefficient
Pg = hydrostatic pressure in the glomerular capillaries
Pb = hydrostatic pressure in Bowman's space
piG = oncotic pressure in glomerulus
piB = oncotic pressure in Bowman's space
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6
Q

Cardiac Pressures

A 
Right atrium: 0-8 mmHg
Right ventricle: 4-25 mmHg
Pulmonary artery: 9-25 mmHg
Left atrium: 2-12 mmHg
Left ventricle: 9-130 mmHg
Aorta: 70-130 mmHg
  • left press > right press
  • atria press max close to 10 mmHg
  • RV max press about 25 mmHg
  • within PA normally close to 25 mmHg
  • LV and aorta press close to systolic press
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7
Q

11beta-hydroxylase

A

conversion of 11-deoxycortisol to cortisol

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8
Q

21 hydroxylase

A
  1. progesterone to 11-deoxycortisone in glomerulosa

2. 17-OH progesterone to 11-deoxycortisol in fasciculata

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9
Q

17alpha-hydroxylase

A
  1. pregenolone to 17-OH pregenolone
  2. progesterone to 17-OH progesterone

both are glomerulosa –> fasciculata

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10
Q

beta-galactosidase

A

lysosomal enzyme responsible for breakdown of glycosaminoglycans

deficiency –> accumulation of keratin sulfate in lysosomes –> short stature, normal intellect, atlantoaxial instability, valvular heart disease

also breaks down lactose

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11
Q

aldolase B deficiency

A

hereditary fructose intolerance

symptomatic after ingesting sucrose and fructose-containing foods the first time, typically as infant

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12
Q

Glucose-6-phosphatase

A

last step in glucose production via gluconeogenesis and glycogenolysis

deficiency causes glycogen storage type 1 disease (von Gierke’s disease)
-sx = hypoglycemia, lactic acidosis, hepatomegaly, hypertriglyceridemia

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13
Q

Thiamine

A

vitamin B1

cofactor for enzymes involved in glucose metabolism:

  • pyruvate dehydrogenase
  • alpha-ketoglutarate dehydrogenase
  • transketolase
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14
Q

Pyruvate dehydrogenase

A

converts pyruvate into acetyl CoA

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15
Q

alpha-ketoglutarate dehydrogenase

A

citric acid cycle

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16
Q

transketolase

A

hexose monophosphate pathway

converts pentoses (derived from glucose) to glyceraldehyde 3P (intermediate in glycolysis)

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17
Q

Pentose phosphate pathway

A

G6PD = rate-limiting step

NADPH production and function

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18
Q

Methylmalonic acid

A

product of fatty acid oxidation

converted to succinyl CoA by methylmalonyl CoA mutase which uses B12 as a cofactor

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19
Q

secretin

A

produced by duodenal S-cells and released in response to inc duodenal H+

stimulates pancreatic ductal cells to inc HCO3- secretion in order to neutralize acidity of the gastric contents entering the duodenum

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20
Q

pancreatic “juice”

A

isotonic secretion

Na and K in same concentration as plasma
HCO3- higher than in plasma
Cl- lower than in plasma (bc Cl and HCO3 are exchanged for each other at apical surface of pancreatic duct cell)

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21
Q

pancreatic enzyme release

A

prompted by CCK and cholinergic stimulation

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22
Q

PNMT

A

phenylethanolamine-N-methyltransferase

conversion of NE to E in adrenal medulla

action augmented by cortisol therefore things dampening production of cortisol lead to dec E in serum

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23
Q

catecholamine breakdown enzymes

A

COMT: NE –> normetanephrine, E –> metanephrine
MAO: normetanephrine and metanephrine –> vannilylmandelic acid

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24
Q

Renin

A

stimulated by decreased sodium delivery to distal tubule, low BP, and beta-1 sympathetic activity (e.g. low intravasc volume)

released by juxtaglomerular apparatus

converts angiotensinogen to angiotensin I in liver

release inhibited by beta blockers

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25
Q

Angiotensin II

A

Effect:

  • type 1 AII receptors: vasoconstriction (systemic arterioles, efferent arteriole), aldosterone secretion in adrenal cortex
  • aldo mediated inc Na reabsorption –> raises BP –> negative feedback –> stops renin release
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26
Q

ACE

A

in lungs

converts AI to AII

degrades bradykinin which normally would cause bronchoconstriction

27
Q

Bradykinin

A

inc prostaglandin production –> bronchial irritation –> coughing

28
Q

how does carotid sinus massage work

A

baroreceptors located at bulges in the internal carotid arteries (i.e. carotid sinus) are constantly firing

inc pressure –> inc firing –> signals to the brain to inc PS influence on heart and vessels

*counterintuitive but think of it as you’re overwhelming the system and brain gets signal to dampen HR, BP, etc.

29
Q

S-adenosyl-methionine

A

ATP + methionine –> SAM (“the methyl donor man”) –> homocysteine and anabolic pathways

regeneration of methionine and SAM is dep on B12 and folate

needed SAM to convert NE –> E

30
Q

Name the four things that inc contractility and SV

A
  1. Catecholamines (inc Ca pump in sarcoplasmic reticulum)
  2. inc intracellular Ca2+
  3. dec extracellular Na+ (dec activity of Na/Ca exchanger by dec the Na gradient that drives its removal of Ca from the cell)
  4. Digitalis (blocks Na/K pump - inc intracellular Na - dec Na/Ca exchanger activity - inc Ca intracellularly)
31
Q

Name the five things that dec contractility and SV

A
  1. beta blockade (dec cAMP)
  2. Heart failure (systolic dysfunction)
  3. Acidosis
  4. hypoxia/hypercapnea (dec PO2 / inc CO2)
  5. Non-dihydropyridine CCBs (eg verapamil, diltiazem)
32
Q

Starling Curve

A

y-axis CO or SV
x-axis Ventricular EDV (preload)
*illustrates that force of contraction is proportional to the end diastolic length of cardiac muscle fiber (preload)

Exercise inc contractility and therefore see left shift

CHF and CHF + digoxin have dec contractility therefore shifted to the right (less so with the latter)

33
Q

Ejection fraction

A

EF = SV/EDV = (EDV - ESV) / EDV

normal >55%

34
Q

Resistance =

A

driving pressure / flow = (8viscositylength) / (pi*r^4)

arterioles = most of total peripheral resistance and regulate capillary flow

35
Q

S3

A

in early diastole during rapid ventricular filling phase

associated with inc filling pressures:

  • MR
  • CHF
  • dilated ventricles –> normal in children and pregnant women
36
Q

S4

A
  • “atrial kick”
  • in late diastole
  • high atrial pressure

associated with ventricular hypertrophy (“left atrium must push against stiff LV”)

37
Q

Normal splitting

A

Expiration | | |
S1 A2 P2
Inspiration | | |

inspiration –> drop in intrathoracic pressure –> inc venous return to the RV –> inc RV stroke volume –> inc RV ejection time –> delayed closure of pulmonic valve

also inc capacity of pulmonary circulation contributes to delayed pulmonic valve closure

38
Q

Wide splitting

A

Expiration | | |
S1 A2 P2
Inspiration | | |

seen in conditions that delay RV emptying (eg pulmonic stenosis, RBBB)

basically exaggeration of physiologic splitting bc delayed RV emptying causes delayed pulmonic sound regardless of breath

39
Q

Fixed splitting

A

Expiration | | |
S1 A2 P2
Inspiration | | |

Seen in ASD

ASD –> left-to-right shunt –> inc RA and RV volumes –> inc flow through pulmonic valve such that regardless of breath pulmonic valve closure is delayed

40
Q

Paradoxical splitting

A

Expiration | | |
S1 P2 A2
Inspiration | ||

seen in conditions that delay LV emptying (aortic stenosis, LBBB)

normal order of valve closure is reversed –> on inspiration, P2 closes later and moves closer to A2, paradoxically eliminating the split

41
Q

Torsades de pointes

A

c/b anything that prolongs QT interval

tx w/ MgSO4

Jervell and Lange-Nielsen syndrome = congenital long QT p/w severe congenital sensorineural deafness
-congenital long QT - defective cardiac Na or K channels

42
Q

Aflutter tx

A

Rhythm control:

  • Class IA
  • Class IC
  • Class III

Rate control:

  • beta blockers
  • CCBs
43
Q

Infectious cause of 3rd degree heart block

A

Lyme disease

44
Q

ANP

A

released from atrial myocytes in response to inc blood volume and atrial pressure

effect:

  • generalized vascular relaxation
  • dec Na reabsorption at medullary collecting tubule
  • constricts efferent renal arterioles and dilates afferent arterioles via cGMP –> diuresis and “escape from aldosterone”
45
Q

Aortic arch receptors

A

transmit signal via vagus nerve to solitary nucleus of medulla

responds only to inc BP

46
Q

Carotid sinus receptors

A

transmit signal via CN IX to solitary nucleus of medulla

responds to dec and inc in BP

47
Q

Cushing reaction

A

*baroreceptor mediated

Triad:

  1. HTN
  2. bradycardia
  3. respiratory depression

inc intracranial pressure constricts arterioles –> cerebral ischemia and reflex sympathetic increase in perfusion pressure (i.e. hTN) –> inc stretch –> reflex baroreceptor induced bradycardia

48
Q

Chemoreceptors

A

Peripheral:

carotid and aortic bodies stimulated by dec PO2 (

49
Q

Right-to-left shunts:

A

5Ts

  1. Tetralogy of Fallot - most common cause early cyanosis
  2. Transposition of the great vessels
  3. Truncus arteriosus - often + VSD
  4. Tricuspid atresia - hypoplastic RV, need ASD and VSD to survive
  5. TAPVR - PVs drain into right heart circulation, assoc with ASD and PDA to allow for right-to-left shunt to maintain CO
50
Q

Left-to-right shunts:

A

Frequency: VSD > ASD > PDA

VSD
ASD (loud S1; wide, fixed split S2)
PDA (close with indomethacin)

51
Q

Eisenmenger’s syndrome

A

uncorrected VSD, ASD, PDA –> pulmonary vascular hypertrophy and HTN

sx = cyanosis, clubbing, polycythemia

52
Q

ToF

A

anterosuperior displacement of the infundibular septum

  1. Pulmonic stenosis
  2. RVH
  3. Overriding aorta (overrides the VSD)
  4. VSD - pulmonary stenosis forces right-to-left shunting –> cyanosis

X-ray shows boot-shaped heart due to RVH

53
Q

transposition of great vessels cause

A

failure of aorticopulmonary septum to spiral

not compatible with life unless there’s a shunt present (VSD, PDA) and early surgical correction is done

54
Q

infantile CoA

A

preductal

assoc with Turner syndrome

55
Q

Adult CoA

A

postductal, i.e. distal to ductus

most commonly assoc with bicuspid aortic valve

p/w rib notching, HTN, upper extremities, weak pulses in lower extremities

56
Q

sequelae of PDA

A

RVH and/or LVH and failure

assoc with continuous “machine-like” murmur

patency maintained by PGE synthesis and low O2 tension –> helpful with ToGV

57
Q

Congenital cardiac defects associated with 22q11 syndromes

A

Truncus arteriosus, ToF

58
Q

Congenital cardiac defects associated with Down syndrome

A

ASD, VSD, AV septal defect

59
Q

Congenital cardiac defects associated with congenital rubella

A

septal defects, PDA, pulmonary artery stenosis

60
Q

Congenital cardiac defects associated with Turner’s

A

preductal CoA

61
Q

Congenital cardiac defects associated with Marfan’s

A

AR, aortic dissection

62
Q

Congenital cardiac defects associated with infant of diabetic mother

A

ToGV

63
Q

arteriosclerosis

A

2 types:

  1. hyaline (thickening of small arteries in essential hTN or DM
  2. hyperplastic (“onion-skinning” in malignant HTN)
64
Q

atherosclerosis histology

A

fibrous plaques and atheromas in INTIMA of arteries

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