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PPP Flashcards

1
Q

What is nebulin?

A

Molecule that extends from Z band along the length of one thin actin filament

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2
Q

What is titin?

A

Associated with myosin filaments extending from Z disk to M line

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3
Q

What is concentric contraction?

A

Contraction stage with an increase in the interdigitation of the filaments

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4
Q

What is eccentric contraction?

A

Stretched stage where I and H bands are wide. Thick and thin filaments do not interact

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5
Q

How is contraction of skeletal muscle initiated?

A

ACh binds to nicotinic receptor at motor end plate; depolarisation spreads into T-tubules –> DHP is activated –> RyR are linked and activated –> release of Ca2+ from sarcoplasmic reticulum; Ca2+ binds to troponin –> change in tropomyosin allowing myosin heads to attach –> contraction

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6
Q

How is extracellular space defined?

A

Plasma + interstitial space

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7
Q

How is total body water distributed?

A 
Plasma space (5% bw; 3.5 L)
Interstitial space (15% bw; 10.5 L)
Intracellular space (40% bw; 28 L)
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8
Q

What is the amount of CSF in the body?

A

Around 150 ml

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9
Q

What substances are used to measure fluid compartments?

A

Plasma volume: albumin, evans blue, labeled inulin
ECS: 24Na, sucrose
TBW: 3H20

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10
Q

What is the difference between osmolarity and osmolality?

A

Osmolarity: 1 osmole per liter
Osmolality: 1 osmole per kg

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11
Q

What is the osmolarity of plasma?

A

290 mosmol/l

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12
Q

What is crystalloid osmotic pressure?

A

Due to small diffusible ions

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13
Q

What is the ionic composition of plasma and intracellular compartment?

A 
Na+: 140 mM and 10 mM
K+: 4 mM and 120/140 mM
Ca2+: 2 mM and around 100 nM
Cl-: 110 mM
bicarbonate: 24 mM
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14
Q

Which are the plasma proteins?

A

Albumin: oncotic pressure of around 25 mmHg
Alpha, beta and gamma globulins
Fibrinogen

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15
Q

What is the count of RBCs and Hb?

A

RBCs: 5.5/4.8 x 10^12 per litre
Hb: 160/140 g per litre

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16
Q

What is the total WBCC?

A

4-11 x 10^9 per litre
Lymphocytes (20-40%)
Monocytes (2-8%)
Granulocytes: neutrophils (50-70%), eosinophils, basophils

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17
Q

What is the total number of platelets?

A

150-400 x 10^9 per litre

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18
Q

What is the normal MCV?

A

85 fL

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19
Q

What are the average pressures in the pulmonary and systemic circulation?

A

Pulmonary: 16 mmHg
Systemic: 92 mmHg

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20
Q

What is Fick’s law?

A 
Rate of diffusion depends on:
1. Area
2. Difference in concentrations
3. Distance over which it has to travel
How easily it diffuses depends on:
1. Temperature
2. Solubility
3. Square root of molecular weight
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21
Q

What is Darcy’s law?

A

Flow = (P1-P2)/R

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22
Q

What is Poiseuille’s law?

A

R = 8VL/pir^4

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23
Q

What is the Fahraeus-Lindqvist effect?

A

Axial streaming due to laminar flow reduces viscosity of blood

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24
Q

How is Rtotal calculated in series and in parallel?

A

Series: Rtotal = R1 + R2 +…
Parallel: 1/Rtotal = 1/R1 + 1/R2 +…

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25
Q

How do you calculate MABP?

A

MABP = CO*TPR

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26
Q

What is the definition of voltage?

A

A measure of the electrical work done to separate charges across the membrane

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27
Q

What is the equilibrium potential?

A

When the force of the concentration gradient of K+ out of the cell is matched by the electrical force pulling K+ back into the cell

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28
Q

What is the Nerst equation for monovalent ions?

A

E = 58 (mV) x log [Cout]/[Cin]

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29
Q

What are the equilibrium potentials of sodium and postassium?

A

Sodium: +50 mV
Potassium: -90 mV

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30
Q

How do you calculate the driving force on the ion out of the cell?

A

Vm - Eeq

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31
Q

What is the Goldman Hodgkin Katz equation?

A

Calculates membrane potential taking into account permeabilities of ions

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32
Q

Where are cardiac t-tubules absent?

A

Atria, neonatal and avian hearts

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33
Q

How long is the cardiac AP?

A

200-400 ms

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34
Q

Why is the cardiac AP so long?

A

Prevents tetany, protects against re-entering arrhythmias

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35
Q

What does cardiac muscle require to initiate contraction?

A

Calcium influx

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36
Q

What is the difference in the mechanisms of calcium release in skeletal, cardiac and smooth muscle?

A

Skeletal: depolarization-induced calcium release (L-type calcium channels/DHP act as plug on RyR)
Cardiac: Ca-induced Ca-release
Smooth: IP3

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37
Q

How is calcium removed from the sarcoplasm in cardiac muscle cells?

A

Through SERCA and sarcolemma Na/Ca exchanger

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38
Q

What is the explanation of the length-tension relationship in cardiac muscle?

A
  1. Overlap of thick and thin filaments (only accounts for 20%)
  2. Increased calcium affinity to troponin C upon increased sarcomere length
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39
Q

What is the Frank Starling law of the heart?

A

CO is directly related to filling pressure; peak systolic pressure is directly related to resting fibre length

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40
Q

How is the force-frequency relationship in a failing heart?

A

Negative: force decreases with increasing frequency; due to decreased action of SERCA and increased action of Na/Ca exchanger

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41
Q

Which are the smooth muscle containing organs?

A

Blood vessels, GI tract, bladder, ureters, urethra, uterus, respiratory system, vas deferens and corpus cavernosum, iris and ciliary body

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42
Q

What are dense bodies?

A

Structures in SMCs that anchor actin filaments

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43
Q

Which are the vasoconstrictors of vascular smooth muscle?

A

Noradrenaline (from symp nerves)
Histamine (locally released from veins), PGF, TXA2
Adrenaline, angiotensin II, vasopressin (hormones)
Pressure, moderate cold

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44
Q

Which are the vasodilators of vascular smooth muscle?

A

VIP, substance P, CGRP, ACh (ANS nerves)
PGE2, PGI2, NO, EDHF, histamine (arterioles)
Adrenaline (some organs), ANP
Flow, heat

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45
Q

How is vascular smooth muscle contraction mediated?

A

Adrenaline/angiotensin II or other vasoconstrictors –> activate alpha 1 receptors:

  1. Phospholipase C –> IP3 and DAG –> calcium release from SR + Ca and Na influx through receptor gated channel
  2. Rho kinase –> calcium sensitisation

Stretch –> stretch activated channel –> sodium influx –> membrane depolarisation –> opening of voltage gated calcium channels (VGCC)

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46
Q

How does NO-mediated vasodilation occur?

A

Endothelial cells secrete NO –> activation of guanylate cyclase –> cGMP:

  1. Stimulation of SERCA and PMCA (plasma membrane Ca ATPase)
  2. Calcium desensitisation
  3. Opening of K+ channels –> membrane hyperpolarisation –> closing of VGCC
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47
Q

How does cAMP-mediated vasodilation occur?

A

Adrenaline, adenosine or prostacyclin –> beta1 activation –> increase in cAMP:

  1. stimulates SERCA and PMCA
  2. Opening of K+ channels –> membrane hyperpolarisation –> closing of VGCC
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48
Q

What are the mechanisms of the crossbridge cycle in SM and its regulation?

A

Myosin light chain kinase + calmodulin + calcium –> active complex:
1. myosin –> phosphorylated myosin –> crossbridge cycle

Regulation by myosin phosphatase:

  1. Inhibited by agonists via rho kinase –> Ca sensitisation
  2. Activated by NO via cGMP –> Ca desensitisation
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49
Q

What are latch bridges?

A

Form when myosin is dephosphorylated while still bound to actin –> cycle very slowly and thus maintain force

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50
Q

What is the AP upstroke and repolarisation in smooth muscle due to?

A

Upstroke: voltage gated calcium channels influx
Repolarisation: K+ outflow

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51
Q

What is the difference between unitary and multi-unit smooth muscle?

A

Unitary: not all cells have synaptic input, excitation is spread through gap junctions
Multi-unit: each muscle cell has synaptic input (iris, ciliary body, piloerector muscles)

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52
Q

Which receptors are present in the sympathetic and parasympathetic pathways?

A

Preganglionic onto postganglionic: ACh onto nicotinic
Postganglionic onto effector:
1. Sympathetic: NA onto alpha or beta (except sweat glands –> ACh onto muscarinic)
2. Parasympathetic: ACh onto muscarinic

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53
Q

What are NA and Adrenaline derived from?

A

Tyrosine + tyrosine hydroxulase –> DOPA
DOPA + DOPA decarboxylase –> dopamine
dopamine + dopamine beta-hydroxylase –> noradrenaline

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54
Q

How and why is NA stored?

A

Unprotected monoamines (NA, serotonin, dopamine) are metabolised by monoamine oxidase (MAO); thus, NA is taken into vesicles via vesicular monoamine transporter (VMAT)

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55
Q

What is the action of reserpine?

A

Blocks VMAT

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56
Q

What is the function of alpha 2 receptors in NA signalling?

A

Located on the presynaptic membrane and provide negative feedback mechanism to prevent further release of NA

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57
Q

What is the action of cocaine?

A

Blocks uptake 1 channels preventing NA reuptake –> more NA is available for signalling

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58
Q

What is the action of clonidine and its uses?

A

alpha2 receptor agonist –> inhibits NA release

Uses: hypertension and tachycardia

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59
Q

How is NA inactivated?

A
  1. Taken up presynaptically by uptake 1 channels –> MAO

2. Diffuses away and is taken up by extrasynaptic uptake (uptake 2) –> COMT –> MAO in liver and gut –> VMA in urine

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60
Q

What are the actions of salbutamol and salmeterol?

A

beta2 agonists –> bronchodilation (asthma) and uterine relaxation

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61
Q

What are the actions and uses of propanolol?

A

non-selective beta antagonist; used for hypertension, angina

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62
Q

What are the actions and uses of prazosin and tamsulosin?

A

Alpha adrenoreceptor antagonist –> benign prostatic hypertrophy

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63
Q

What are the effects of alpha1 stimulation on the following:

  1. Vascular smooth muscle
  2. Longitudinal muscle of GI tract
  3. Anal sphincter
  4. Urinary sphincter
  5. Uterine muscle
  6. Radial muscle
  7. Salivary glands
  8. Glycogen metabolism
  9. Vas deferens
A
  1. Vascular smooth muscle: contraction
  2. Longitudinal muscle of GI tract: relaxation
  3. Anal sphincter: contraction
  4. Urinary sphincter: contraction
  5. Uterine muscle: contraction
  6. Radial muscle: contraction
  7. Salivary glands: increased secretion
  8. Glycogen metabolism: increase
  9. Vas deferens: contraction
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64
Q

What are the effects of beta1 stimulation?

A

Increased heart rate and force of contraction

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65
Q

What are the effects of beta2 stimulation?

A

Relaxation of bronchial smooth muscle and vascular smooth muscle
Skeletal muscle, coronary and hepatic arteriole vasodilation
Uterine smooth muscle relaxation
Glycogen mobilisation in the liver

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66
Q

How do adrenaline and noradrenaline sympathomimetics differ in their action?

A

Noradrenaline: more potent on alpha receptors, least on beta2
Adrenaline: more potent on beta receptors, used also for anaphylactic shock (im or sc)
Both used for acute hypotension and cardiac arrest (iv)

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67
Q

Which are alpha-selective sympathomimetics?

A

phenylephrine (alpha1): acute hypotension

clonidine (alpha2): hypertension, migraine

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68
Q

Which are beta-selective sympathomimetics?

A

Isoprenaline (beta): heart block
Salbutamol: asthma, premature labor
Dobutamine: cardiogenic shock

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69
Q

What are labetalol and carvedilol?

A

non-selective adrenergic receptor antagonists

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70
Q

What are propanolol and timolol?

A

beta-selective antagonists

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71
Q

What are metaprolol and atenolol?

A

beta1-subtype selective antagonists

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72
Q

What are the structures of muscarinic and nicotinic receptors?

A

Muscarinic:
-GPCR
-5 subtypes: M2 (cardiac) –> Galphai/o leads to decrease in cAMP; M3 (smooth muscle, glandular) –> increase in IP3 and DAG
Nicotinic: nonselective cation channel, causes rapid cell depolarisation –> 5 subunits and 2 subtypes

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73
Q

How does the baroreceptor reflex work?

A

Arterial stretch sensed by afferent nerves of vagus nerve (aortic arch) and glossopharyngeal nerve (carotids) –> signal to the NTS in brain stem:
1. increase PNS drive to heart –> decrease heart rate and CO
2. decrease SNS –> decreased TPR
since BP = CO*TPR –> BP decreases

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74
Q

What are the parasympathetic effects on the eye?

A

Accommodation for near vision –> contraction of ciliary muscle allows lens to relax
Pupil constriction –> contraction of sphincter pupillae muscle in the iris (pupil constriction)
Mediated by CN III (oculomotor nerve)

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75
Q

What are the mechanisms of cholinergic neurotransmission?

A 
Choline acetyltransferase:
Acetyl CoA + choline --> acetylcholine
Storage in vesicles
Acetylcholinesterase:
ACh --> choline + acetate --> reuptake mechanism
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76
Q

Why is ecothiopate given for closed angle glaucoma?

A

long-lasting cholinesterase inhibitor:

pupillary constriction increases outflow of acqueous humour –> decreased intraocular pressure

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77
Q

What is the action of botulinum toxin?

A

Binds to and degrades SNAP-25 –> prevents exocytosis of ACh and other NTs

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78
Q

How is salivary secretion controlled?

A

Afferents from smell, higher brain centres to hypothalamus and from trigeminal nerve (tongue) to brain stem:

  1. Parasympathetic efferents: CN IX to parotid and VII to sublingual and submandibular
  2. Sympathetic: through thoracic nerves I and II
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79
Q

Where is innervation to the GI tract located?

A

Submucosa: Messner’s plexus

Between inner circular and outer longitudinal: Auberbach’s plexus

80
Q

How do parietal cells work?

A

Activated H+/K+ ATPase by increase in cAMP –> canaliculi formation –> Cl- follows H+ through facilitated diffusion
Cl- enters cell at basolateral membrane through Cl-/HCO3- antiporter

81
Q

How does the gastric phase of gastric acid secretion work?

A

Distension of the stomach:
1. ENS –> ACh –> stimulation of antral G cells, ECL cells and parietal cells
2. Vagovagal reflex –> ACh release + GRP (gastrin releasing peptide) –> stimulation of antral G cells –> gastrin –> ECL cells –> histamine –> parietal cells)
Digestion of protein:
1. peptides and amino acids stimulate antral G cells

82
Q

What enzymes are present in the pancreatic juice?

A

Proteolytic: trypsinogen, chymotrypsinogen, procarboxypolypeptidase, ribonuclease, deoxyribonuclease
Amylase
Lipase

83
Q

How are trypsinogen and chymotrypsinogen activated in the intestinal lumen?

A

Enterokinase: trypsinogen –> trypsin
Trypsin: chymotrypsinogen –> chymotrypsin

84
Q

How are carbohydrates digested?

A

Pancreas and salivary glands secrete alpha-amylase: starch –> maltose + glucose
Small intestine secretes 1,6-glucosidase
Small intestine contains maltase, lactase and sucrase

85
Q

How are proteins digested?

A

Stomach: HCl activates pepsinogen –> pepsins
Pancreatic juices: carboxypeptidases, trypsin, chymotrypsin
Small intestine: breakdown tri and dipeptides with aminopeptidases and dipeptidases; absorption through Na+ and H+ (tri and dipeptide) co-transport

86
Q

How is bile secretion regulated?

A

PNS through vagus nerve –> production of bile in liver
Acidic chyme sensed by enteroendocrine cells of duodenum:
1. Secretion of secretin in the blood –> flow of bile rich in HCO3- and pancreatic juices
Fatty acids and amino acids in chyme:
2. Secretion of CCK –> contraction of gall bladder

87
Q

What is bile flow dependent on?

A

partial pressure of O2

88
Q

What is the structure of the biliary tree?

A

Apical membranes of hepatocytes form canaliculi –> terminal bile ductules (canals of Hering) –> perilobular ducts –> interlobular ducts –> septal ducts –> lobular ducts –> left and right hepatic ducts –> common hepatic duct + cystic duct –> common bile duct

89
Q

How does the gallbladder concentrate bile acids?

A

Apical membrane:
1. Na-H and Cl-HCO3- exchangers –> reabsorption of NaCl
Basolateral membrane:
1. Na/K+ pump –> Na+ exits
2. Cl- leaves through channels
Additional:
1. H2O and HCO3- move through leaky junctions from lumen into blood
Result: isotonic bile with higher concentration of bile acids

90
Q

How is bilirubin excreted?

A

85% from breakdown of red blood cells; fat soluble and toxic; bound to albumin in blood; free form taken up by the liver –> formation of bilirubin glucuronide –> secretion into bile canaliculi
15% reabsorbed in the intestine

91
Q

How are lipids absorbed?

A

Glycerol, short-chain and medium-chain FAs: pass through enterocyte and enter capillaries
Cholesterol, lysophospholipids, long-chain FAs and monoglycerides: present in lumen as mixed micelles with bile salts –> allows absorption of fatty acids at brush border (low pH) –> SER, combine with apoproteins from RER to form chylomicrons (apo B48, C-II, E) or VLDLs –> Golgi –> lacteals

92
Q

What is the function of cholesterol ester transfer protein?

A

Transfer cholesterol esters from HDL to VLDLs, IDLs or LDLs

Cholesterol esters in HDL are formed by LCAT

93
Q

How does the breakdown of fat work?

A

Lingual lipase
Breakdown in stomach (10-30%): gastric lipase + emulsification by gastric contractions
Breakdown and micelle formation in duodenum and jejunum (70-90%): pancreatic lipase
Absorption in small intestine
Excretion as Ca2+ soaps (5%)

94
Q

What is the enterohepatic circulation of bile acids?

A

Bile acids are primarily conjugated to taurine or glycine to form bile salts –> secreted into the duodenum and then:

  1. Reabsorbed passively as conjugated bile salts or through Na+-coupled transporters in terminal ileum
  2. Bacteria in terminal ileum and colon deconjugate –> passively absorbed by nonionic diffusion
  3. Bacteria in terminal ileum and colon dehydroxylate –> secondary bile salts –> passively reabsorbed or excreted in faeces
95
Q

What are the causes of gallstones?

A
  1. too much absorption of water from bile
  2. too much absorption of bile acids
  3. too much cholesterol in bile
  4. inflammation of epithelium
96
Q

What are the effects of vagal and splanchnic nerve stimulation on bile secretion?

A

Vagus: increase production and secretion

Splanchnic nerve: vasoconstriction and reduced flow of bile

97
Q

What is function of VIP on bile secretion?

A

Inhibits net fluid and electrolyte absorption in gallbladder

alpha adrenergic blockage of neural VIP increases fluid absorption

98
Q

What is the role of GIP?

A

inhibition of gastric acid secretion + stimulation of insulin secretion; produced by K cells of the duodenum and jejunum

99
Q

What is the function of the chorda lingual nerve?

A

Parasympathetic innervation evokes marked fluid secretion accompanied by increased blood flow and oxygen consumption

100
Q

What is the function of atropine on salivary excretions?

A

Atropine blocks secretion but not blood flow (VIP or substance P co-release)

101
Q

How is salivation controlled?

A

Production of watery saliva is elicited by cholinergic, adrenergic and peptidergic stimulation
Sympathetic innervation: initial vasoconstriction (then vasodilation) with a viscous, protein-rich secretion via beta-adrenergic stimulation

102
Q

What is the structure of the salivary tree?

A

Acinar cells –> ductule-striated or intercalated ducts –> larger ducts –> main excretory duct into the mouth

103
Q

Through which pathways do sympathetic and parasympathetic nerves operate on salivary glands?

A 
Sympathetic:
1. Beta1 --> increased cAMP and NO
2. Alpha1 --> increased Ca2+
Parasympathetic:
1. VIP --> increased cAMP and NO
2. ACh --> muscarinic 1, 3 receptors --> increased cAMP
104
Q

How are primary and secondary saliva different?

A

Primary: isotonic to plasma
Secondary: hypotonic to plasma (reabsorption of NaCl + K+ and HCO3- secretion)

105
Q

How is primary saliva produced?

A

NTs and hormones –> increase in intracellular Ca2+ in acinar cells:
1. Activation of K+ channels on basolateral membrane and Cl- channels on luminal
2. Reuptake via Na+-K+-2Cl- cotransporter dependent on Na+/K+ ATPase
Result: Cl- leaves through channels in luminal membrane and draws water and Na+ through paracellular space

106
Q

What are the two phases of swallowing?

A

Voluntary phase: bolus and tongue movements

Involuntary phase: reflex response stimulated by mechanoreceptors (CN IX and X)

107
Q

How do gastric secretions vary between cardia, pyloric and oxyntic glands?

A

Cardiac glands: mucous primarily, few or no peptic or oxyntic cells
Pyloric glands: alkaline mucous juice and some electrolytes (Ca phosphate, NaCl, KCl and bicarbonates)
Oxyntic glands: key site of gastric HCl secretion

108
Q

What are the different types of cells in gastric pits and what is their function?

A

Superficial epithelial cells
Mucous neck cells: HCO3- rich mucous secretion
Stem/regenerative cells
Parietal/oxyntic cells: HCl secretion
Chief cells: pepsinogen production and secretion
Endocrine G cells: gastrin secretion

109
Q

What is the Dimaline model as opposed to the Soll’s three receptor model?

A

Gastrin activates CCK2 on ECL-cell –> histamine is released and acts on H2 receptors on parietal cells –> cAMP increase
Other pathways:
1. Direct activation of parietal cells by gastrin (CCK2 receptors)
2. ACh activation by M3 receptors –> increase in Ca2+

110
Q

What are the functions of famotidine and omeprazole?

A

Famotidine: H2 antagonist
Omeprazole: proton pump inhibitor

111
Q

How is gastrin secretion regulated?

A

D-cells sense acid in stomach and release somatostatin which inhibits G-cells

112
Q

What is the intestinal phase of gastric secretion?

A

Protein digestion products stimulate acid secretion:
1. Intestinal G cells –> gastrin
2. Intestinal endocrine cells –> entero-oxyntin –> G-cell stimulation
3. Absorbed amino acids –> G cell stimulation
Intestinal acid, fat and hyperosmolar solutions inhibit acid secretions:
1. receptors for H+, osmolarity and neutral amino acids –> sympathetic inhibition
2. fat –> secretion of SIH, GIP and secretin –> endocrine inhibition

113
Q

What are the characteristics of pancreatic juice and how is it secreted?

A

HCO3- and NaCl-rich isotonic fluid

  1. Basolateral uptake of Cl- through NKCC
  2. Basolateral exit of Na+ through Na+/K+ ATPase and exit of K+ through channels (stimulated by Ca2+)
  3. Cl- diffuses down electrochemical gradient at apical membrane
  4. Na+ follows paracellularly
  5. HCO3- produced by carbonic anhydrase –> diffusion and/or HCO3/Cl- exchanger
114
Q

Is the GI tract single or multi-unit smooth muscle?

A

Single (gap junctions are present)

115
Q

What are the interstitial cells of Cajal?

A

Act as pacemakers in the GI tract

116
Q

What is the effect of vagal stimulation, CCK, GIP and secretin on gastric motility?

A

Vagal stimulation: increases
CCK: decreases
GIP: decreases
secretin: decreases

117
Q

Which has the fastest spontaneous activity: stomach, duodenum, ileum or colon?

A

Duodenum

118
Q

What is the function of motilin?

A

Regulates migrating motor complex from stomach to intestines

119
Q

Which mechanisms regulate gastric emptying?

A

Neural enterogastric reflex:
1. Short reflexes operate via ENS
2. Long reflexes via CNS (increase symp and inhibit parasymp)
Hormonal mechanisms:
1. Secretin (stimulates HCO3- secretion and inhibits stomach activity)
2. CCK (gallbladder contraction and inhibits stomach activity)
3. GIP (inhibits gastric contractions)
4. Motilin (increases gastric and intestinal motility)

120
Q

What are the crypts of Lieberkuhn?

A

Opening of intestinal glands

121
Q

Which cells are present in the villous epithelium?

A

Goblet cells and absorptive cells

122
Q

What is the function of Paneth cells?

A

Key effectors of innate mucosal defense of intestinal crypts

123
Q

How is absorption of monosaccharides driven?

A

Basolateral Na+/K+ ATPase generates sodium gradient –> allows SGLUT to work

124
Q

How is the absorption of oligopeptides through H+ cotransporter driven?

A

Apical Na+/H+ exchanger pumps H+ outside –> creates gradient
Basolateral Na+/K+ ATPase pumps Na+ outside –> creates gradient

125
Q

What are hartnup disease and cystinuria?

A

Hartnup disease: autosomal-recessive –> reduced absorption of neutral amino acid phenylalanine
Cystinuria: autosomal recessive –> reduced absorption of L-cystine and cationic amino acids (L-arginine)

126
Q

What are the differences between alpha and gamma tocopherol?

A

Alpha: resecreted as component of hepatically derived HDL and VLDLs
Gamma: metabolised and excreted by the liver

127
Q

How are vitamins B and C absorbed?

A

B1, 2: sodium cotransporter in jejunum

C: sodium cotransporter in ileum

128
Q

How is calcium absorbed across intestinal epithelium?

A

Facilitated diffusion from lumen –> bound to calbindin intracellularly –> exits basolateral membrane via:

  1. Ca2+/3Na+ exchanger
  2. Ca2+/H+ ATPase
129
Q

What are Brunner glands?

A

Situated in the duodenum –> secrete alkaline or neutral mucous

130
Q

Which hormones act on the kidneys?

A

ADH, aldosterone, natriuretic peptides, parathyroid hormones, fibroblast growth factor 23 (FGF23)

131
Q

Which hormones are produced by the kidneys?

A

Renin, vitamin D, erythropoietin, alphaKlotho, prostaglandins

132
Q

What is the filtration interface of the renal corpuscle composed of?

A 
Fenestrated capillary endothelium
Basement membrane (fixed polyanions)
Tubular epithelium (podocytes)
133
Q

What are the types of nephrons and their prevalence?

A

Cortical (85%), juxtamedullary (15%)

134
Q

What constitutes the juxtaglomerular apparatus?

A

Macula densa (end of ascending loop of Henle)
Mesangial cells in between the afferent and efferent arteriole
Juxtaglomerular cells on afferent arteriole (innervated by sympathetic fibers)

135
Q

How much of the plasma that enters the glomerulus is filtered?

A

20%

136
Q

What is a substance that is filtered and secreted but not reabsorbed?

A

PAH

137
Q

What are substances that are filtered and some of it are reabsorbed?

A

Water and electrolytes

138
Q

What is a substance that is filtered and completely reabsorbed?

A

Glucose

139
Q

What is the maximal size for glomerular filtration?

A

7 kDa

140
Q

What are the differences between ultrafiltrate and plasma?

A

Ultrafiltrate does not contain proteins and molecules that can bind to proteins (Ca2+ and some drugs)
Albumin binds acidic drugs, alpha1-acid glycoprotein binds basic drugs

141
Q

What is the definition of GFR?

A

Volume of fluid filtered from the glomeruli per minute

142
Q

What is the net glomerular filtration pressure?

A

(60-15)-(29-0)= 16 mmHg

143
Q

What are the typical GFR and urine output?

A

GFR: 180 l/day

urine output: 1.5 l/day

144
Q

How is filtered glucose reabsorbed and where?

A

PT;

  1. SGLT
  2. GLUT facilitated transporters
  3. Na+/K+ ATPase keeps gradient
145
Q

How are amino acids reabsorbed and where?

A

PT;
at least 8 aa transporters, 6 Na+-dependent
Proteins: reabsorbed through endocytosis

146
Q

How are phosphate and sulphate reabsorbed in PCT?

A

Na+ coupled transporters

147
Q

Which compounds are passively reabsorbed in PCT?

A

urea, chloride, potassium, calcium

bicarbonate (linked to H+ secretion)

148
Q

Which compounds are secreted in PCT?

A

Organic acids (anions): enter basolateral through dicarboxylate exchange (OAT1,3; Na+ coupled transport with DC-), exit via ATP-dependent transporters
1. Drugs (penicillin)
2. Endogenous molecules (bile salts, fatty acids, prostaglandins)
3. diagnostic agent (PAH)
Organic bases (cations): enter via facilitated organic cation transporter (OCT2), exit through MATEs antiporter in exchange for H+ or OCTN
1. Endogenous molecules (creatinine, dopamine, choline, guanidine, histamine, serotonin, adrenaline)
2. Drugs (morphine, atropine)

149
Q

What is the definition of clearance?

A

Volume of plasma that is cleared of a substance in a given time (uv/p)

150
Q

Which substances are used to measure GFR?

A

Experimentally: inulin (filtered, not secreted, not reabsorbed)
Clinically: creatinine

151
Q

How do you measure renal plasma flow?

A

renal plasma flow = PAH clearance (around 600 ml/min)

152
Q

How do you calculate blood flow from plasma flow?

A

Blood flow = plasma flow/ (1-hematocrit)

153
Q

What are the normal osmolalities for plasma and urine?

A

Plasma: 285-295 mosom/kg
Urine: 50-1400 mosm/kg

154
Q

Where is the majority of sodium reabsorbed?

A

Proximal (65%) and thick (25%) ascending

Hormonal control: distal (2-5%) and collecting (5%)

155
Q

How is sodium reabsorbed in proximal tubule?

A 
Apical:
1. Na/H exchanger 
2. Na-nutrient symporter
Basolateral:
Na+/K+ ATPase
Others: Cl- follows paracellularly
156
Q

How is sodium reabsorbed in the thick ascending limb?

A 
Apical:
1. NKCC
2. K+ channels --> pump K+ out to create gradient
Basolateral:
1. Na/K+ ATPase
2. KCl cotransporter
3. Cl- channels
157
Q

How is sodium reabsorbed in the distal tubule?

A 
Apical:
1. NaCl cotransporter
Basolateral:
1. Na/K+ ATPase
2. Cl- channels
3. K+ channels
158
Q

How is sodium reabsorbed in the collecting duct?

A

Principal cells (Na+ transport), intercalated cells (H+ transport)
Apical: eNaC
Basolateral: Na+/K+ ATPase

159
Q

How does the loop of henle work?

A

Countercurrent multiplier
Descending limb: picks up salt and loses water (AQP1) –> progressively more concentrated
Ascending limb: solute pump, water-impermeable –> dilute urine (100 mosm/kg)
Vasa recta: countercurrent exchange mechanism

160
Q

How does urea recycling by the kidney occur?

A
  1. PT: passive reabsorption of urea (50%)
  2. Loop of henle: apical secretion via urea transporters (UT-A2) –> 60% secreted
  3. Inner medullary collecting duct (apical reabsorption via UT-A1 + UT-A3) –> 70% reabsorbed
    40% of that filtrated is excreted
161
Q

What is the action of ADH on collecting duct?

A

ADH stimulates GPCR –> increase cAMP –> activated PKA –> AQP2 expression on apical side
AQP3 and 4 on basolateral

162
Q

What is the definition of oliguria?

A

Output below 0.428 l/day

163
Q

What are the definitions of concentrated and dilute urine?

A

Dilute: <300 mosm/kg
Concentrated: >300 mosm/kg

164
Q

How is osmolar clearance calculated?

A

Cosm = (Uosm*V)/Posm

165
Q

What is the free water clearance?

A 
Reflects the ability of the kidneys to excrete concentrated or dilute urine
Ch2o = V- Cosm
>0 --> hypo-osmotic
=0 --> isosmotic
<0 --> hyperosmotic
166
Q

What are the regions involved in ADH release?

A

Osmoreceptors in OVLT, MPN, SFO signal to supraoptic nuclei (SON) and paraventricular nuclei (PVN) in hypothalamus –> ADH release from posterior pituitary

167
Q

Which molecules increase/decrease ADH secretion?

A

Angiotensin II increases; natriuretic peptides decreases
Alcohol –> inhibits ADH
Nicotine –> stimulates ADH

168
Q

What is diabetes insipidus?

A
  1. urination (polyuria –> >2l/day)
  2. thirst (polydipsia)
  3. nocturia
    Neurogenic: no ADH secreted
    Nephrogenic: inherited mutation in channel or acquired
169
Q

What is osmotic diuresis?

A

Increased urination due to small molecules in renal tubule lumen

170
Q

What are the elements involved in the maintenance of potassium balance?

A

Renal excretion, GI losses, cellular shifts

171
Q

How much potassium is ingested daily?

A

40-120 mmoles

172
Q

How is potassium filtered, reabsorbed and secreted in urine?

A

800 mmoles/day is filtered

95% passively reabsorbed (65% passively in PT, 30% in thick ascending limb, 5% in distal tubule via K+/H+ exchanger)

173
Q

How do collecting ducts influence K+ reabsorption and secretion?

A

Intercalated cells: K+ reabsorbed through K+/H+ exchanger

Principal cells: K+ is secreted by ROMK, Ca2+ activated big-conductance K+ channels (BK) and KCl cotransporter

174
Q

Which factors affect K+ secretion by principal cells?

A
  1. Factors affecting Na+ entry through ENaC
  2. Aldosterone stimulates K+ channels
  3. Tubular flow rate: high flow favours secretion
  4. Acid-base balance: acidosis inhibits, alkalosis enhances
175
Q

What is hypokalemia and what are its causes?

A

K+ < 3.5 mM

  1. Increased external losses (diuretics, hyperaldosteronism, alkalosis, vomiting, diarrhoea, burns, intense sweating)
  2. redistribution into cells (metabolic alkalosis, insulin excess)
  3. Inadequate K+ intake
176
Q

What is hyperkalemia and what are its causes?

A

K+ > 5.5 mM
1. Decreased external losses (renal failure, hypoaldosteronism, action of drugs)
2. Redistribution out of cells (acidosis, lack of insulin, tissue destruction)
Treatment: Ca2+ iv, insulin administration, long-term diuretics

177
Q

What is the lateral preoptic area responsible during water deprivation?

A

Osmoreceptors –> signal thirst

178
Q

What are the intrinsic and extrinsic controls of GFR?

A

Extrinsic: maintains arterial BP by controlling GFR (sympathetic NS baroreceptor reflex)
Intrinsic: protects renal capillaries from hypertensive damage (tubuloglomerular feedback)

179
Q

How does the tubuloglomerular feedback work?

A

Increased flow of Na through macula densa –> increased production of adenosine –> increased Ca2+ in granular juxtaglomerular and VSM cells –> constriction and inhibition of renin release

180
Q

What stimuli lead to renin release?

A
  1. low sodium delivery to macula densa
  2. decreased wall tension in afferent arteriole (intrarenal baroreceptor)
  3. sympathetic activity
  4. low blood volume (hypovolemia)
181
Q

What are the effects of renin?

A 
Plasma angiotensinogen --> Angiotensin I
Angiotensin I + ACE --> angiotensin II:
1. Stimulates PT Na+ reabsorption
2. ADH release
3. Aldosterone secretion
4. Thirst
5. Vasoconstriction of small arterioles
182
Q

What stimuli lead to aldosterone secretion?

A

Angiotensin II; increased K+ concentration

183
Q

What are natriuretic peptides?

A

Released when the heart is stretched; A type from atrial myocardium and B type from ventricular myocardium
Actions:
1. Inhibit Na+ entry through ENaC in principal cells and Na/K ATPase in proximal tubule
2. inhibit renin release and aldosterone production
3. Inhibit ADH release
4. Systemic vasodilation –> decreased BP
5. Afferent arteriole dilation –> increased GFR

184
Q

What are the buffers in blood, extracellular, intracellular fluid and urine?

A

Blood: hemoglobin, bicarbonate and plasma proteins
Extracellular fluid: bicarbonates, very little proteins
Intracellular fluid: intracellular proteins, phosphates, a little bicarbonate
Urine: ammonia, phosphates

185
Q

How does the kidney control pH?

A
  1. Absorb HCO3-

2. Excrete H+

186
Q

Where does bicarbonate reabsorption occur?

A

PT, ascending loop of Henle, intercalated cells type A
H2O + CO2 + carbonic anhydrase –> H+ + HCO3-:
bicarbonate goes to blood
H+ secreted into filtrate –> not excreted if HCO3- is available in the lumen

187
Q

How does H+ excretion happen?

A

In combination with nonbicarbonate buffer (monohydrogen phosphate)
Result: addition of new HCO3- to plasma

188
Q

Apart from H+ excretion, what is another mechanism that produces new HCO3-?

A

Glutamine absorbed through Na+ symport into tubular epithelium
Glutamine metabolised in tubule epithelium –> ammonium ions + bicarbonate
Ammonium ions secreted through Na+ exchanger

189
Q

What is the difference between respiratory and metabolic acidosis and alkalosis?

A

Respiratory acidosis: high pCO2
Respiratory alkalosis: low pCO2
Metabolic acidosis: low HCO3-
Metabolic alkalosis: high HCO3-

190
Q

How is acidosis compensated?

A
  1. Chemical: CO2 –> HCO3-
  2. Brainstem: adjust ventilation
  3. Renal mechanisms: increase plasma HCO3-
191
Q

How is metabolic alkalosis compensated in the kidneys?

A

Type B intercalated cells secrete HCO3- through HCO3-/Cl- exchanger

192
Q

How does glutamine production by the liver change in alkalosis and acidosis?

A

Acidosis: increases
Alkalosis: decreases

193
Q

How is the epithelium of the colon?

A

Flat with deep crypts

194
Q

What is the percentage of water in normal stool?

A

65-85%

195
Q

How does intestinal Na+ reabsorption vary throughout the GI tract?

A

Proximal bowel: Na/H exchanger
Jejunum: SGLUT, Na-aa cotransport
Ileum: NaCl cotransport
Colon: Na+ ion channels + HCO3-/Cl- antiporter

196
Q

What types of diarrhoea are there?

A

Congenital: deficiency of normal ion transport system (Cl-/HCO3- exchanger lacking)
Bacterial infection: cholera toxin –> permanently activates AC –> increased cAMP –> Cl- secretion
Osmotic (>350 mosm)

197
Q

Which bacteria are present in the colon?

A

Bacteroides: gram-negative, anaerobic, non spore forming
Bifidobacteria: “good bacteria”, gram-positive, non-sporeforming, lactic acid bacteria

FBS1 (5 decks)

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