Physiology Flashcards
MAP
(SBP + 2DBP) / 3
CO x Total Peripheral Resistance
CO =
SV + HR
rate of O2 consumption / (arterial - venous O2 content)
CO at rest and exercise
5 L/min –> 20 L/min
Renal plasma flow
RPF estimated by calculating paraaminohippuric acid (PAH) clearance
filtration fraction FF = GFR / RPF
GFR calculation
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
Cardiac Pressures
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
11beta-hydroxylase
conversion of 11-deoxycortisol to cortisol
21 hydroxylase
- progesterone to 11-deoxycortisone in glomerulosa
2. 17-OH progesterone to 11-deoxycortisol in fasciculata
17alpha-hydroxylase
- pregenolone to 17-OH pregenolone
- progesterone to 17-OH progesterone
both are glomerulosa –> fasciculata
beta-galactosidase
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
aldolase B deficiency
hereditary fructose intolerance
symptomatic after ingesting sucrose and fructose-containing foods the first time, typically as infant
Glucose-6-phosphatase
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
Thiamine
vitamin B1
cofactor for enzymes involved in glucose metabolism:
- pyruvate dehydrogenase
- alpha-ketoglutarate dehydrogenase
- transketolase
Pyruvate dehydrogenase
converts pyruvate into acetyl CoA
alpha-ketoglutarate dehydrogenase
citric acid cycle
transketolase
hexose monophosphate pathway
converts pentoses (derived from glucose) to glyceraldehyde 3P (intermediate in glycolysis)
Pentose phosphate pathway
G6PD = rate-limiting step
NADPH production and function
Methylmalonic acid
product of fatty acid oxidation
converted to succinyl CoA by methylmalonyl CoA mutase which uses B12 as a cofactor
secretin
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
pancreatic “juice”
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)
pancreatic enzyme release
prompted by CCK and cholinergic stimulation
PNMT
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
catecholamine breakdown enzymes
COMT: NE –> normetanephrine, E –> metanephrine
MAO: normetanephrine and metanephrine –> vannilylmandelic acid
Renin
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
Angiotensin II
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
ACE
in lungs
converts AI to AII
degrades bradykinin which normally would cause bronchoconstriction
Bradykinin
inc prostaglandin production –> bronchial irritation –> coughing
how does carotid sinus massage work
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.
S-adenosyl-methionine
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
Name the four things that inc contractility and SV
- Catecholamines (inc Ca pump in sarcoplasmic reticulum)
- inc intracellular Ca2+
- dec extracellular Na+ (dec activity of Na/Ca exchanger by dec the Na gradient that drives its removal of Ca from the cell)
- Digitalis (blocks Na/K pump - inc intracellular Na - dec Na/Ca exchanger activity - inc Ca intracellularly)
Name the five things that dec contractility and SV
- beta blockade (dec cAMP)
- Heart failure (systolic dysfunction)
- Acidosis
- hypoxia/hypercapnea (dec PO2 / inc CO2)
- Non-dihydropyridine CCBs (eg verapamil, diltiazem)
Starling Curve
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)
Ejection fraction
EF = SV/EDV = (EDV - ESV) / EDV
normal >55%
Resistance =
driving pressure / flow = (8viscositylength) / (pi*r^4)
arterioles = most of total peripheral resistance and regulate capillary flow
S3
in early diastole during rapid ventricular filling phase
associated with inc filling pressures:
- MR
- CHF
- dilated ventricles –> normal in children and pregnant women
S4
- “atrial kick”
- in late diastole
- high atrial pressure
associated with ventricular hypertrophy (“left atrium must push against stiff LV”)
Normal splitting
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
Wide splitting
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
Fixed splitting
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
Paradoxical splitting
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
Torsades de pointes
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
Aflutter tx
Rhythm control:
- Class IA
- Class IC
- Class III
Rate control:
- beta blockers
- CCBs
Infectious cause of 3rd degree heart block
Lyme disease
ANP
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”
Aortic arch receptors
transmit signal via vagus nerve to solitary nucleus of medulla
responds only to inc BP
Carotid sinus receptors
transmit signal via CN IX to solitary nucleus of medulla
responds to dec and inc in BP
Cushing reaction
*baroreceptor mediated
Triad:
- HTN
- bradycardia
- 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
Chemoreceptors
Peripheral:
carotid and aortic bodies stimulated by dec PO2 (
Right-to-left shunts:
5Ts
- Tetralogy of Fallot - most common cause early cyanosis
- Transposition of the great vessels
- Truncus arteriosus - often + VSD
- Tricuspid atresia - hypoplastic RV, need ASD and VSD to survive
- TAPVR - PVs drain into right heart circulation, assoc with ASD and PDA to allow for right-to-left shunt to maintain CO
Left-to-right shunts:
Frequency: VSD > ASD > PDA
VSD
ASD (loud S1; wide, fixed split S2)
PDA (close with indomethacin)
Eisenmenger’s syndrome
uncorrected VSD, ASD, PDA –> pulmonary vascular hypertrophy and HTN
sx = cyanosis, clubbing, polycythemia
ToF
anterosuperior displacement of the infundibular septum
- Pulmonic stenosis
- RVH
- Overriding aorta (overrides the VSD)
- VSD - pulmonary stenosis forces right-to-left shunting –> cyanosis
X-ray shows boot-shaped heart due to RVH
transposition of great vessels cause
failure of aorticopulmonary septum to spiral
not compatible with life unless there’s a shunt present (VSD, PDA) and early surgical correction is done
infantile CoA
preductal
assoc with Turner syndrome
Adult CoA
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
sequelae of PDA
RVH and/or LVH and failure
assoc with continuous “machine-like” murmur
patency maintained by PGE synthesis and low O2 tension –> helpful with ToGV
Congenital cardiac defects associated with 22q11 syndromes
Truncus arteriosus, ToF
Congenital cardiac defects associated with Down syndrome
ASD, VSD, AV septal defect
Congenital cardiac defects associated with congenital rubella
septal defects, PDA, pulmonary artery stenosis
Congenital cardiac defects associated with Turner’s
preductal CoA
Congenital cardiac defects associated with Marfan’s
AR, aortic dissection
Congenital cardiac defects associated with infant of diabetic mother
ToGV
arteriosclerosis
2 types:
- hyaline (thickening of small arteries in essential hTN or DM
- hyperplastic (“onion-skinning” in malignant HTN)
atherosclerosis histology
fibrous plaques and atheromas in INTIMA of arteries