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CO formulas (SV, HR, MAP, TPR)

CO = SV x HR
MAP = CO x TPR (P = Q x R)


Pulse pressure formula

5 causes of increased pulse pressure
3 causes of decreased pulse pressure

pulse pressure = systolic pressure - diastolic pressure

Increases: hyperthyroidism, AR, aortic stiffening, OSA, exercise
Decreases: AS, post-MI shock, cardiac tamponade


What 3 factors change stroke volume?

CAP: contractility, afterload, preload


What 3 factors increase contractility? CND

catecholamines: increased Ca pump in SR, therefore increased [Ca]i

decreased [Na]e: decreased activity of Na/Ca exchanger (increased [Ca]i)

Digoxin: decreased Na/K pump --> incr. [Na]i --> decreased Na/Ca, incr. [Ca]i


What 4 factors increase myocardial oxygen demand?

increased with CARD: contractility, afterload, rate, diameter of ventricle

increased with wall tension (which = P x r / 2 x thickness)

increased afterload --> increased wall thickness to decrease wall tension and decrease O2 demand


What value approximates preload?

- approximated by ventricular EDV
- depends on venous tone, circulating blood volume


What value approximates afterload?

- approximated by MAP


Starling curve axes

stroke volume or CO vs. ventricular EDV

note: a left shift (increased CO for a given EDV) corresponds to an increase in contractility


Systemic resistance (R)

Give formulas and facts

P = Q x R (R = P/Q)
Q = v x A

capillaries are highest cross-sectional area, lowest velocity

arterioles form the majority of TPR (organ removal = increased TPR, lead to decreased CO)


CO/preload interplay
(inotropy, venous return, TPR)

Inotropy: alters CO for a given preload
Venuos return: alters preload for a given CO
TPR: altered CO for a given preload

exercise: incr. inotropy, decr. TPR = increased CO
fluid retention: decr. inotropy, incr. preload = increased CO (to compensate for HF)


Contraction phase cycle

(graph shows relationship between LV pressure vs. LV volume)

1: isovolumetric contraction
2: systole
3: isovolumetric relaxation
4: diastole

increased contractility = decr. ESV (higher SV), left expansion
increased preload = incr. EDV (higher SV), right expansion
increased afterload = increased ESV (lower SV), narrowing from the left


Heart sounds

S1: mitral/tricuspid closure
S2: atrial/pulmonic closure
S3: increased flow velocity in early diastole (due to dilated ventricular chamber)
S4: heard in late diastole due to atrial kick


JVP waveforms

a = atrial contraction
c = RV contraction
x = atrial relaxation
v = filling of right atrium
y = right atrium emptying into right ventricle


JVP characteristics on physical exam

multiphasic, non-palpable, occludable


S2 splitting (normal, wide, fixed, paradoxical)
aortic vs. pulmonic valve closure

normal: incr. venous return w/ inspiration --> delayed PV closure
wide: pulm stenosis, RBBB --> delayed RV emptying
fixed: ASD --> const. incr. RV volume --> delayed PV closure

paradoxical: aortic stenosis, LBBB --> delayed aortic closure (pulmonic closes first! therefore paradoxical), gap closes on inspiration instead of widening


L sternal border auscultation

best for diastolic murmurs (eg. AR), or hypertrophic cardiomyopathy


Effects of bedside maneuvers
Hand grip
Rapid squatting

Inspiration: incr. venous return, incr. intensity of R heart sounds
Hand grip: incr. afterload, incr. intensity of MR/VR/VSD
Valsalva (phase 2): decr. preload, incr. hypertrophic cardiomyopathy
Rapid squatting: incr. venous return, increased AS murmur, decr. hypertrophic cardiomyopathy


Systolic heart murmurs
Aortic stenosis
Mitral regurg
Mitral valve prolapse

AS: Crescendo-decrescendo (peripheral pulse is late and weak)
MR: holosystolic blowing
MVP: late systolic crescendo w/ click
VSD: holosystolic, harsh


Diastolic heart murmurs

Describe sounds

AR: high-pitched blowing
MS: opening snap, rumbling late


Myocardial action potential

Phase 0: depol = opening of fast Na channels (influx)
Phase 1: inactivation of Na channels, opening of K channels (efflux)
Phase 2: opening of Ca channels (influx, L type), plateau
Phase 3: rapid repol, close of Ca channels, opening of slow K channels (efflux)
Phase 4: resting = K+ ep. pot., high K permeability


Cardiac vs. skeletal potentials

1.) Plateau in cardiac cells
2.) SR initiates in skeletal
3.) cardiac nodal cells spontaneously depolarize due to funny current
4.) cardiac myocardium are electrically coupled through gap junctions


Pacemaker cell potentials

Phase 0: upstroke, opening of Ca
Phase 3: Ca inactivate, then incr. K efflux
Phase 4: slow Na influx (funny current slowly depolarizes)


Funny current variables

Ach/adenosine = decreased HR
catecholamines = increased HR


Congenital long QT syndrome

usually due to ion channel defects

sometimes seen with deafness


Brugada syndrome

Asian males, pseudo-RBBB, V1-V3 ST elevation
due to ion channel defect
tx: ICD



both: act via cGMP to vasodilate and decrease Na resorption by the kidney

ANP: increase with blood volume
BNP: increase with ventricular torsion


Aortic vs. carotid receptors

Aortic: located in arch, transmit through CN X
Carotid: located at bifurcation, transmit through CN IX

both to solitary nucleus in medulla


Baroreceptors stimulation

firing increases with stretch!

decreased stretch --> decr. firing --> incr. symp activation (BP, HP, etc.)


Carotid massage mechanism

Incr. pressure on carotid sinus = incr. stretch/incr. firing = incr. AV refractory period = decr. HR


Cushing reflex (incr. ICP, incr. BP, decr. HR)

incr. ICP --> cerebral ischemia --> incr. PCO2 --> symp reflex --> incr. BP --> incr. stretch --> decr. HR


Chemoreceptors (peripheral vs. central)

Peripheral: stimulated by decr. PO2, incr. PCO2, decr. blood pH

Central: pCO2, respond to levels in the brain interstitial fluid (CO2 flows better to bloodstream)


Insulin synthesis

Preproinsulin then...

RER: cleavage of signal peptide to proinsulin, folded and formation of disulfide bonds

Transport to Golgi

Immature granules: cleavage into insulin and C-peptide

Insulin packaged in mature granules for secretion


Insulin receptor

- bind tyrosine kinase receptors


Insulin secretion

Glucose enters B-cell through GLUT2
Increased ATP/ADP ratio closes K channel (less K efflux)
Depolarization leads to Ca influx (acitvates phospholipase C, increased IP3 to further increase intra Ca)
High [Ca]i leads to granule release


Prolactin function and regulation

- function: leads to milk production, decr. ovulation/spermatogenesis by decr. GnRH

- hypothalamus secretes DA (inhibits prolactin) and TRH (stimulates prolactin)
- prolactin inhibits GnRH, stimulates DA


GH function and secretion

linear growth, muscle mass and insulin resistance

Stimulated by GHRH during sleep and exercise


Appetite regulation
Ghrelin vs. Leptin

Ghrelin - stimulates hunger and GH release, produced by stomach

Leptin - satiety, produced by adipose, low in starvation, mutation = obesity


ADH synthesis and function

synthesized in supraoptic nucleus
V2 receptors: regulate serum osmolarity
V1 receptors: blood pressure

secretion regulated by osmoreceptors in the hypothalamus


17-OHase deficiency (decr. androstenedione)

- blocks progenitors from cortisol/sex hormone production, only aldosterone is made

- def = incr. aldosterone (incr. BP, K+ wasting), decr. sugar/sex hormones


21-hydroxylase deficiency (incr. 17-OH-P)

2nd step in aldosterone/cortisol synthesis

- def = increased sex hormones, decr. salt/sugar hormones (decr. BP, high serum K+)


11B-hydroxylase deficiency

3rd step in salt/sugar hormone synthesis

- def = incr. 11-DOH-C (incr. BP, K+ wasting), decreased aldosterone/cortisol, increased sex hormones


Cortisol functions (BIG FIB)

increase in: Blood pressure (incr. alpha receptors = incr. sens. to Epi/NorEpi), Insulin resistance, Gluconeogenic

decrease in: Fibroblast activity, Inflammatory/Immune responses, Bone building


Albumin-bound Ca and pH

increased pH (more basic) = more neg. charge on albumin = more bound Ca --> hypocalcemia


Vit. D effects

increased absorption of Ca and PO4 from gut
increased bone resorption from Ca and PO4

regulation: stimulated by PTH, low Ca, low PO4


PTH effects (give target organs, molecular mediators, and stimulators)

leads to increased serum Ca, decreased serum PO4

- kidney: incr. Vit. D, incr. Ca, decr. PO4 (so urine will have low Ca and high PO4)
- bone: release of Ca and PO4 (osteoclasts by RANK-L)

- increased MCSF and RANK-L

- stimulated by low Ca, high PO4, low Mg


Calcitonin effects

opposes PTH

tones down Ca levels by decreasing bone resorption of Ca


Sex-hormone binding globulin (effects of incr./decr. levels)

increased SHBG --> decr. free testosterone --> gynecomastia

decreased SHBG --> incr. testosterone --> hirsutism

pregnancy and OCPs increase SHBG levels


Thyroid hormones (effect on metabolism, effects of T3)

- control metabolic rate through Na/K ATPase activity (and thus O2 consumption)

T3: Brain maturation, Bone growth, B-adrenergic effects, Basal metabolism

TBG: decr. in hepatic failure, incr. in pregnancy


Iodine and thyroid hormones

T4 is converted to T3 by 5'-deiodinase (PTU blocks this also)

Thyroid peroxidase prepares idoine to be incorporated in T3 (PTU blocks this)


Gastrin (G cells in antrum)

Effects and secretion

increased H+ secretion, mucosa, motility

stimulated by food in the stomach

abnormally increased in H. pylori, Z-E, PPI use


Somatostatin (D cells in pancreas, mucosa)

decr. acid, decr. pancreatic/gall bladder secretions, decr. insulin/glucagon

Stimulated by acid


Cholecystokinin/CCK (I cells in duodenum)

increased pancreatic secretions, delayed stomach emptying

acts on neural muscarinics


Secretin (S cells in duodenum)

incr. HCO3, bile, decr. gastric acid

Allows for enzyme function in the duodenum


GIP (K cells in duodenum)

exocrine: decr. H+
endocrine: incr. insulin


motilin (small intestine)

incr. MMCs!



incr. water/electrolyte secretion

stimulated by vagal nerve


Parietal cell inputs and mechanisms for acid secretion

Ach, gastrin --> Gq --> IP3
histamine* --> Gs --> cAMP
Both increased H+/K+ ATPase

Prostaglandins, somatostatin --> Gi --> decr. cAMP


Gastric acid regulation

Stimulated by histamine, Ach, gastrin

Inhibited by somatostatin, GIP, prostaglandins


Pepsin (chief cells)

Protein digestion

vagal stimulation

pepsinogen --> pepsin in the presence of H+


HCO3- (mucosal cells and Brunner glands)

Neutralize acid

Is secreted and then trapped in the mucus lining the epithelium


Pancreatic secretions (give the 3 enzymes)

amylase - starch digestion
proteases are secreted as zymogens
trypsinogen - activates other proenzyes, requires activation by enterokinase and peptidase


Carbohydrate absorption (give 3 glucose transporters)

Monosaccharides only through SGLT-1 (Na-dependent)
Fructose through GLUT-5
Transferred to bloodstream through GLUT-2


D-xylose test

if intact mucosa, then absorbed and excreted in urine
if SIBO/Whipple's, then decr. absorption and treated with Abx
if still not fixed, then structural deformity (eg. celiac)


Peyer patches

M-cells: APCs
B-cells transform to IgA-secreting plasma cells in the lamina propia


Bile production (give rate limiting step and three functions)

rate-limiting step: cholesterol 7-a-hydroxylase

functions: digestion, cholesterol excretion, anti-microbials



macs: heme --> unconj. bilirubin (bound to albumin in blood)

liver: unconj. bili + albumin --> conj. bili

gut: conj. bili --> urobilinogen (20% reabsorbed, 10% of which is secreted in urine and 90% of which is sent back to liver in enterohepatic circulation)

liver enzyme: UDP-gluconyltransferase


Give the Xa inhibitors
Give the IIa (thrombin) inhibitors

Xa inhibs: LMWH*, heparin, rivaroxaban, fondaparinux

IIa inhibs: heparin*, LMWH, argatroban


Give type and factor affected

All have lack of functional clotting factors

A: decr. 8
B: decr. 9
C: decr. 11


Describe the clotting pathways

Intrinsic: [12 --> 11 --> 9] --> 10 --> 2 (thrombin) --> 1 (fibrin)
Extrinsic: [7 --> 10]

Note: 8 (9 -->10) and 5 (10 --> 2) both require Ca and phospholipid


Platelet plug formation (give 5 steps and notable factors)

Injury: transient vasoconstriction
Exposure: vWF (WP bodies, alpha granules) binds exposed collagen
Adhesion: plts adhere by GpIb, release ADP, Ca, TxA2
Activation: ADP in plt --> GpIIb/IIIa
Aggregation: fibrinogen binds GpIIb/IIIa, links plts


Give thrombotic (platelet) anticoagulants

Aspirin = decr. COX-1 --> decr. TxA2
Clopidogrel = decr. GpIIb/IIIa


Ristocetin assay

normally ristocetin activates vWF to bind Gp1b

failure of agglutination during assay = vWF disease or Bernard-Soulier (decr. plt adhesion)


Describe 3 platelet defects

Glanzmann - decr. GpIIb/IIIa (decr. activation)
vWF disease
Bernard-Soulier - decr. GpIb (decr. adhesion)


Glomerular filtration (give 3 components of the barrier)

1.) fenestrated endothelium (size barrier)
2.) BM w/ heparan (neg. charge)
3.) podocyte foot processes


Clearance formula

Cx = (Ux times V) / Px
in words, clearance is equal to urine conc. times urine flow rate all over plasma conc.

If Cx > GFR, then net secretion
If Cx < GFR, then net reabsorption



GFR = Cinulin (inulin has no net secretion or reabsorption)

Also, GFR = Kf[(Pgc - Pbc) - (πgc - πbc)]

Normal = 100 mL/min

Creatinine overestimates due to slight secretion (clearance is abnormally elevated)


Effective renal plasma flow

eRPF = Cpah (PAH is freely filtered and secreted)

RBF = RPF/(1 - Hct)

- note: underestimated by 10%


Filtration fraction formula

FF = GFR /RPF (normal = 20%)
in words, the proportion of fluid entering kidney that then enters the tubules
This has to be manipulated in situations where the blood flow to the kidney itself is variable


Afferent/efferent arteriole physiology

Afferent dilation (prostaglandins): increased GFR/RPF, no effect on FF

Afferent constriction (symp NS): decreased GFR

Efferent constriction (Ang. II): decr. RPF, incr. GFR, incr. FF)


Glucose in the kidney

mainly reabsorbed in PCT by Na/glucose co-transporter

>200 = glucosuria, >375 = saturation of transporters


Hartnup disease (amino acid transport)

Decreased AA transporters in the PCT --> neutral aminoaciduria

Leads to decr. tryptophan --> decr. niacin --> PELLAGRA

Tx: high-protein diet


Proximal tubule

give function and two compounds that act here

reabsorb glucose/AA/HCO3/Na/Cl/PO4/K/H20
- secretes NH4+ to maintain luminal charge

Ang II: incr. Na/H exchange, incr. Na/H2O/HCO3 absorption
Acetazolomide: decr. carbonic anhydrase --> decr. HCO3 reabsorption


Thin descending loop of Henle function

Water reabsorption according to medullary gradient

- aka concentrating segment



Thick ascending loop function

- Na/K/Cl reabsorption
- also, induced paracellular reabsorption of Ca/Mg

NO H2O transport!


Distal Convoluted Tubule

reabsorb Na/Cl
- site of the MOST DILUTE URINE

- PTH: increased Na/Ca reabsorption on basal/blood side


Collecting tubule

Give details of aldosterone/ADH effects

- reabsorb Na, secrete K

Aldosterone: nuclear receptor, increased mRNA to increased Na/K pump and ENaC on principal cell. Loss of lumen positivity leads to K wasting

ADH: through V2 receptors, leads to increased aquaporins on apical side


Fanconi anemia effects and causes

Generalized reabsorptive defects

Increased excretion of everything --> metabolic acidosis (Type 2/proximal RTA)

Causes: Wilson's, ischemia, multiple myeloma


Bartter syndrome defect and effects

defect in Na/K/2Cl transporter in ascending limb

leads to hypokalemia, metabolic alkalosis, and hypercalciuria


Gitelman syndrome defect and effects

defect in Na/Cl transporter in DCT

less severe than Bartter


Liddle syndrome defect and effects

gain of function mutation in ENaC

- leads to hypertension, hypokalemia

tx: amiloride (ENaC inhibitor)


Apparent mineralocorticoid excess

11 B-OH dH leads to failure of cortisol --> cortisone

incr. cortisol --> activation of MC receptors

leads to HTN, K wasting

- acquired from licorice


RAAS sensors

1.) JG cells (respond to low BP) secrete renin
2.) macula densa (respond to low distal Na delivery) release adenosine
3.) B1 receptors (respond to incr. symp drive)


RAAS function

increased renin cleaves angiotensinogen to AT-1

ACE (from pulmonary endothelium) cleaves AT-1 to AT-2 (also breaks down bradykinin)


Effects of angiotensin-2 (six total)

Vasoconstriction: AT1 receptor of vascular smooth muscle

Efferent arteriole constriction: increased FF/GFR to preserve renal function

Aldosterone: principal cells (incr. ENaC, basal Na/K pump), alpha-intercalated (H+ ATPases)

ADH: increased aquaporins

PCT: incr. Na/H activity (incr. Na/HCO3, H2O reabsorption)

hypothalamus: stimulates thirst


Atrial natriuretic peptide

- acts on afferent arteriole to increase GFR
- also decreases Na reabsorption in the DCT


Renal tubular acidoses

(give name, location, electroytes involved)

Type I distal: alpha-intercalated, no new HCO3, decr. H secretion, assoc. with hypokalemia

Type II proximal: decr. PCT HCO3 reabsorption, hypokalemia

Type IV hyperkalemic: hypo-aldosterone leads to excess K, decreased NH4 secretion
- can be either an absolute reduction in aldosterone or aldosterone resistance


Estrogen sources and hormone secreted

Ovary: estradiol
Adipose: estrone
Placenta: estriol

Estradiol > estrone > estriol


Estrogen receptor

Expressed in cytoplasm

Translocates to nucleus when bound by estrogen


Estrogen functions

Development, increased estrogen/LH/progesterone receptors

increased SHBG, incr. HDL, decr. LDL

Incr. endometrial proliferation


Progesterone sources

Corpus luteum, placenta, adrenal cortex, testes


Progesterone function

stimulate endometrial glands and spiral arteries

Production of thick cervical mucus

incr. body temp, decr. endometrial proliferation



primary oocytes: 2N, 4C, frozen in prophase I until ovulation (46 sister chromatids)
secondary oocytes: 1N, 2C, frozen in metaphase II until fertilization (23 sister chromatids)



Sperm entering oocyte triggers cortical reaction (prevention of another sperm from entering, continuation of second division, leading to extrusion of polar body)



increased estrogen past the inhibitory threshold leads to an LH surge, which induces ovulation (follicle rupture) and progesterone-induced rise in temperature

Fertilization must happen within 1 day, in the ampulla


Lactation (describe roles of prolactin and oxytocin)

Prolactin - induces milk production, decreases reproductive potential

Oxytocin - assists in milk letdown, promotes uterine contractions


hCG (give source and function)

source: syncytiotrophoblasts

function: maintian corpus luteum for first 8-10 weeks

incr. in twins, Down's, moles
decr. in ectopic, Edward/Patau



full cycle takes 2 months

spermatogonium: 2N, 2C (46 chromosomes), then become... (after leaving blood-testis barrier)

primary spermatocyte: 2N, 4C (46 sister chromatids)
secondary spermatocyte: 1N, 2C (23 sister chromatids)

Spermatid: 1N, 1C, then undergoes maturation (loss of cytoplasmic contents and gain of acrosomal cap) to become spermatozoon


Androgens (potency, function, conversion enzymes)

DHT > testosterone > androstenedione

testosterone: differentiation, growth spurt, voice, libido
DHT: penis, scrotum, prostate (then, balding, sebaceous glands)

5a-reductase: testosterone --> DHT
aromatase: convert androgens to estrogen in adipose tissue (estrogen helps close epiphyseal plates)


Lung volumes

Describe IC, ERV, VC

FRC is the base line (RV + ERV), and a normal breath in is the TV
Maximal inspiration from FRC = TV + IRV = IC
Maximal expiration from FRC = ERV

Maximal inspiration/expiration overall: ERV + TV + IRV = VC (vital capacity)


Physiologic dead space

(give formula as well)

Volume of air that does not participate in gas exchange

= tidal volume times (arterial CO2 - expired CO2)/arterial CO2



taut (low affinity) vs. relaxed (high affinity)

Taut in tissues! Therefore allows O2 unloading
- more taut = R shift (incr. H+, 2-3BPG, temp)

Relaxed in respiration! Therefore allows O2 binding



Oxidized Hb, increased affinity for CN
Causes by nitrites/thiosulfate, which is used to treat CN poisioning



Hb bound to CO, decr. O2 capacity, decr. O2 unloading


Hb dissociation curve (describe shape, shifts)

Hb: positive cooperativity (incr. O2 binding = incr. affinity) leads to higher binding potential

R shift = lower saturation for a given pO2, caused by incr. H+, temp, 2/3BPG


Oxygen content of the blood

Dissolved O2 + (Hb times 1.34 mLO2/gHb times %sat)

Note! O2 delivery = O2 content times CO


Pulmonary circulation

normally, low resistance with incr. compliance

Note, opposite reactivity from systemic circulation; low PaO2 (hypoxemia) --> vasoconstriction


Gas diffusion

In normal resting human: O2 and CO2 are perfusion-limited (PaO2 depends on flow rate)

In emphysema and fibrosis, O2 is diffusion-limited, and therefore doesn't PaO2 does not equal PAO2 by the time blood leaves the capillary


Pulmonary vascular resistance

PVR = pressure in pulm. artery minus pressure in left atrium all divided by cardiac output (recall, R = deltaP/Q)


Alveolar gas equation

PAO2 = PIO2 - PaCO2/RQ = 150 - PaCO2/0.8

normal A-a gradient = 10-15 mmHg
incr. A-a gradient = V/Q mismatch, shunt, diffusion impairment



normal A-a: high altitude, hypoventilation
increased A-a: V/Q mismatch, shunting, diffusion impairment


CO2 transport (Haldane effect, Bohr effect)

90% as HCO3-, 5% as HbCO2, 5% dissolved

When O2 binds to Hb in the lungs, H+ is let go and forms CO2, allowing for unloading and expiration

In peripheral tissue, incr. H+ from metabolism leads to incr. O2 unloading


High altitude effects

incr. ventilation, decr. PaCO2, incr. EPO, incr. 2,3BPG (shift of curve to right)

also, incr. renal excretion of HCO3