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DIG 209 FINAL > Physiology > Flashcards

Physiology Flashcards

1
Q

A) Functions of kidney:

A
  1. Regulation of water & electrolytes balance
  2. Regulation of arterial blood pressure (short term: RAAS & long term: Na– H2O excretion)
  3. Regulation of acid base balance (elimination of acids + regulation of buffer stores)
  4. Excretion of waste (urea & creatinine) and foreign chemicals (drugs & food additives)
  5. Endocrine function (erythropoietin → RBCs, activation of vitamin D3, renin secretion)
  6. Paracrine function (PGs & BK → regulation of RBF)
  7. Gluconeogenesis
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2
Q

Mechanisms of RBF Autoregulation When BP ↑

A

Myogenic mechanism:

↑ BP –> stretch of vascular wall —> open stretch gated Ca++ channels —> Ca++influx —> contraction of smooth muscles of afferent arterioles

Tubuologlomerular feedback:

↑ BP —>↑ RBF & GFR —>↑reabsorption of Na & Cl —> ↑ delivery of solutes into macula densa —>macula secretes adenosine –> acts on receptors —> VC of afferent

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3
Q

Mechanism of RBF autoregulation for when BP↓

A

Myogenic:
↓ BP–> Relaxation of smooth muscles of afferent arterioles

Tubuloglomerular feedback:

↓ BP—> ↓ RBF & GFR—->
↓reabsorption of Na & Cl—-> ↓ delivery of solutes into macula densa —> macula densa: VD of afferent & VC of efferent

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4
Q

Functions of mesangial cells

A
  1. Support glomerular capillaries by mesangial matrix.
  2. Mesangial cells contract —> ↓ filtration surface area.
  3. Phagocytose immune complex & secretes cytokines.
  4. Removes debris and aggregated proteins from glomerular membrane.
  5. Have receptors for vasoactive substances.
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5
Q

Factors affecting GFR

A

Look at booklet

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6
Q

Give the Na reabsorption in the proximal tubule

A

65% of filtered Na is reabsorbed in PCT

First half of PCT: Co transport with AA, glucose, phosphate and sulfate, counter transport Na-H counter transporter

Late half of PCT: Na is reabsorbed with Cl passively

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7
Q

Give the Na reabsorption in the Loop of henle

A

Thin descending limb: Only water reabsorption, No na transporter

Thin ascending limb: No water reabsorption, Na is reabsorbed with Cl passively

Thick ascending limb: 25% of filtered Na is reabsorbed by Co transporter that carries Na, K and Cl. Most K refluxes back into lumen via K channels

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8
Q

Give the Na reabsorption in Distal tubule

A

Early distal tubule: Na is reabsorbed with Cl by NaCl cotransported

Late distal tubule & collecting duct: Less than 10% of filtered Na is reabsorbed prinicpal cells in exchange with K under aldosterone control.

passive diffusion of Na and K in into principal cells

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9
Q

Regulation of Na excretion

A
  1. GFR (glomerulo-tubular balance)
    - ↑GFR —>↑ Na and water reabsorption.
    - Mechanism: renal tubules reabsorb constant percentage of Na rather than constant amount.
    - Importance:
    o Prevent overloading of DCT when ↑GFR
    o Prevent inappropriate loss of Na or water in
  2. Rate of flow: slow rate —> ↑ Na reabsorption
  3. ABP.
    - Pressure diuresis & natriuresis: ↑ GFR —> ↑ Na & water excretion.
    - Mechanism: ↑ ABP —> ↓ Angiotensin II —> ↑ HP in peritubular capillary —-> ↑ HP in renal interstitial fluid —> enhance back leak of Na into tubular lumen –>↓ Na reabsorption & ↑ excretion.
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10
Q

Give the hormonal control for increase of Na reabsorption

A

Aldosterone: ↑ number of Na+ – K+ ATPase pump in basolateral border.

Glucocorticoids: weak mineralocorticoid activity

Angiotensin II: activate aldosterone secretion, Act directly on PCT stimulate Na —- K ATPase pump

Sex hormone: estrogen

Sympathetic stimulation
- VC of afferent. —> ↓ GFR
- Activate renin —> ↑ RAAS
- Increase Na reabsorption by PCT & thick ascending limb of loop of Henle.

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11
Q

Hormones that decrease Na reabsorption

A

ANP: increase NaCl excretion. Relaxation of mesangial cells, VD of afferent & VC of Efferent –> increase GFT —> increase Na filtration & reabsorption

PGE2: inhibit Na–K ATPase & Na channels

Endothelin: increase PGE2

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12
Q

Give an account on the obligatory water reabsorption

A

Proximal tubule: 65% of water is reabsorbed
in proximal tubule by osmosis. Movement of water is facilitated by insertion of aquaporin 1 channels

Loop of Henle:
in descending limb: highly permeable to water by osmosis due to gradual increase in medullary ISF

Early distal tubule & collecting duct: impermeable to water continued dilution of tubular fluid

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13
Q

Give an account on the facultative water reabsorption

A

In late distal tubule & cortical collecting duct:
↑ADH —-> ↑ number of aquaporin 2 channels —> 8% of filtered water is reabsorbed by osmosis into the interstitium of the cortex.

In medullary duct: 4.7% of filtered water is reabsorbed into medullary hypertonic interstitium —> concentrated urine

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14
Q

Give an account on the mechanism producing hyperosmotic renal medullary interstitium

Countercurrent multiplier system (function of juxtamedullary nephrons of loop of Henle)

A

Ascending limb:
Thick segment: active reabsorption of solute
Thin segment: passive reabsorption of NaCl

Descending limb: high permeable to water and less permeable to solutes. Water diffuses from descending limb to medullary interstitium by osmosis

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15
Q

Give an account on the mechanism producing hyperosmotic renal medullary interstitium

Countercurrent exchanger system of vasa recta

A

Descending limb of vasa recta:
Solutes diffuse from medullary ISF into blood along concentration gradient. Water diffuses from blood to ISF

Ascending limb of vasa recta: Solutes diffuse back into medullary ISF along concentration gradient. Water diffuse into vasa recta

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16
Q

Give an account on the mechanism producing hyperosmotic renal medullary interstitium

Contribution of urea

A
  • Urea contributes about 40% of osmolarity of renal medullary ISF.
  • At inner medullary CD–> urea moves into medullary ISF —> adding to hyperosmolarity (movement is facilitated by ADH)
  • High protein diet –> concentrated urine & vice versa.]
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17
Q

Give an account of the disorders of urine concentration

A

Diabetes insipidus: polyuria & polydipsia. Polydipsia keeps the patients alive

Syndrome of inappropriate ADH secretion (SIADH)
Water retention –> ECF expansion.

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18
Q

Compare between water diuresis and osmotic diuresis in causes, mechanism, outcome, ADH

A

Water diuresis: ingestion of large amounts of water. Mechanism: ↑H2O –> ↓ plasma osmolarity –> ↓ ADH —> ↓ facultative reabsorption. Large amount of urine which is very diluted. ADH inhibited

Osmotic diuresis: Large amount of un-reabsorbed solute in tubular fluid.
Mechanism:
a) Un-reabsorbed solutes –> hold water inside tubules –> ↓ obligatory water reabsorption.
b) water retention —>↓ active reabsorption of Na —>↓
Na concentration —> Na retention + ↓ medullary
osmolarity.

Outcome: decrease H2O reabsorption and increase Na
ADH: normal or increased

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19
Q

Give an account on the K handling in renal tubules

A

K reabsorption: 65% in PCT. In thick ascending limn–> its 25%. In DT and CD it is dependent on K intake

K excretion: By principal cells depending on K intake and aldosterone level. In basolateral border K moves by Na/K ATPase. IN luminal border K moves via electrochemical gradient, K channels, and K–Cl co transporter

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20
Q

Give an account on the glucose reabsorption by renal tubules

A

All glucose is reabsorbed in early PCT

At luminal border: Glucose transported with NA with SGLT-2. Glucose is carried against concentration gradient

At basolateral border: Glucose is carried along concentration gradient by GLUT-2

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21
Q

Define tubular transport maximum

A

Tubular transport maximum: maximum amount of actively transported substances that can be reabsorbed per minute

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22
Q

Draw the curve and label each part. Define splay and cause of splay

A

Splay: is the region of reabsorption curve where reabsorption is reaching saturation but not fully saturated

Heterogeneity of the nephrons

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23
Q

Define Glycosuria and give its causes

A

Presence of glucose in urine in large amount

Caused by DM and congenital defect in glucose transport

24
Q

Give the secretion of hydrogen & reabsorption of bicarbonate

A

Reabsorption of bicarbonate: HCO3- is reabsorbed mainly in PCT (85%), thick ascending loop of Henle (10%) & CD (4.8%). CO2 from blood combines with H2O which from a buffer system

Secretion of hydrogen: H is secreted in all parts of renal tubule except of loop on Henle. In PCT, thick parts of loop on Henle & early DCT–>2ry active transport Na —H counter transport.

25
Q

Mentions the importance of hydrogen buffering

A

H secretion occurs as long as pH is > 4.5. IF H not buffered–> limiting pH is reached rapidly–> H secretion stops

26
Q

Factors affecting H secretion

A
  1. aldosterone: ↑ H & K secretion
  2. Intracellular PCO2: high PCO2 —> ↑ H secretion
  3. intracellular K: ↑K intracellularly —> ↓ H secretion & vice versa
27
Q

Mention the pH, reason for, causes and compensation respiratory acidosis.

A

less than 7.4

↑ PCO2

RC depression, air way obstruction, respiratory muscle

Renal: ↑ PCO2—> formation of H & HCO3 from CO2 in tubular cells. H is secreted to tubular fluid & HCO3 is diffuse back to plasma

28
Q

Mention the pH, reason for, causes and compensation in respiratory alkalosis

A

Greater than 7.4

↓ PCO2

High altitudes, fever, hyperventilation

↓ HCO3- Reabsorption + ↓ HCO3- & H+ formation due to ↓CO2

29
Q

Mention the pH, reason for, causes and compensation in metabolic acidosis

A

Less than 7.4

↓ HCO3-

Increase protein intake, severe diarrhea

Renal: ↑ HCO3- generation

30
Q

Mention the pH, reason for, causes and compensation in metabolic alkalosis

A

Greater than 7.4

↑ HCO3-

Vomiting

Renal: ↓ HCO3- Reabsorption & ↑excretion

31
Q

Mention the micturition reflex

A

§ Stimulus: volume of urine in bladder à 300 – 400 ml

§ Receptors: stretch receptors in bladder wall & posterior urethra

§ Afferent: pelvic parasympathetic

§ Efferent: S2 & S3

§ Effector & response: detrusor muscle contraction & internal urethral sphincter relaxation.

32
Q

Give an account on higher center control and give its function

A

Facilitatory (2P): pontine & posterior hypothalamus.

Inhibitory: mid-brain

Faciliatory & inhibitory: cortical micturition center
in superior frontal gyrus.

Functions:
1) Keep micturition reflex partly inhibited except
in desired micturition.

2) Prevent micturition even it occurs –>
contraction of external sphincter.

3) When it is time to urinate–> facilitatory centers
facilitate micturition reflex & inhibit external
sphincter.

33
Q

Give an account on the enteric nervous system

A

2 neural plexuses: myenteric plexus in control of peristalic activity while Submucosal plexus controls exocrine & endocrine secretion

These neurons secrete: NO, ach, serotonin, GABA

34
Q

Explain the site of release, stimuli and actions of gastrin

A

G cells

Distention of stomach, vagal stimulation, chemical stimuli like soup

Simulate gastric motility, increase acid and pepsin secretion

35
Q

Explain the site of release, stimuli and actions of Cholecystokinin-Pancreozymin.

A

APUD cells in upper intestine

Presence of peptide, AA and fat in small intestine

Stimulates pancreatic acini, inhibit gastric motility, enhance intestinal motility, stimulate insulin secretion

36
Q

Explain the site of release, stimuli and actions of secretin

A

APUD cells in upper intestine

decrease pH in intestinal fluid < 4.5

Stimulates pancreatic duct, decrease gastric acid secretion, augment action of CCK

37
Q

Describe Pharyngeal stage of swallowing

A

Stimulus: bolus of food in pharynx
Receptor: pharyngeal opening
Center: in medulla

Response: rapid peristaltic wave in superior then middle then inferior pharyngeal muscles and upper pharyngoesophageal sphincter relaxes

38
Q

Give the stimuli of secretion and actions of gastric inhibitory peptide and Vasoactive intestinal peptide

A

GIP:
Stimuli of secretion: presence of fat and glucose in duodenum
Actions: decrease HCl secretion and stimulate insulin secretion

VIP:
Stimuli of secretion: digestive products in intestine.
Actions: VC of intestinal vessels, inhibit gastric secretion, relaxation of GIT smooth muscles

39
Q

Give the site of release, stimuli secretion, actions of Motilin and Somatostatin (GHIH)

A

Motilin

Stimuli of secretion: digestive products
Actions: Stimulates duodenal motility and contraction of lower esophageal sphincter

Somatostatin (GHIH)

Stimuli of secretion: presence of HCl
Actions: inhibit gastrin, secretin, GIP, VIP. Inhibits gastric acid secretion

40
Q

Describe involuntary Esophageal stage of swallowing?

A
  1. Primary peristaltic wave: continuation of peristaltic wave begins in pharynx, passes all the way from pharynx to stomach in 8 to 10 seconds.
  2. Secondary peristaltic waves: result from distention of the esophagus by the retained food if primary peristaltic wave fails to move all the food into stomach
41
Q

Describe function and control of lower esophageal sphincter

A

Sphincter: remains tonically contracted, in contrast to the mid and upper esophagus

Function: prevent reflux of gastric contents into esophagus (regurgitation)

When peristaltic waves passes down the esophagus –> “receptive relaxation” relaxes LES–> easy food propulsion

Tone of LES under control of Ach, NO & VIP, diet

42
Q

Give the abnormalities of the tone of LES

A

Gastroesophageal reflux: decrease resting tone of LES –> reflux of gastric acid content into esophageal —> heartburn and esophagitis

Achalasia: incomplete relaxation of LES–> accumulation of food—> massive dilation of esophagus.

43
Q

Discuss the regulation of gastric evacuation

A
  1. Gastric factors: Distension of the stomach –> increase emptying via

x Nervous reflexes: long vago-vagal reflexes, short local reflexes
x Hormonal: gastrin

  1. Intestinal factors: decrease emptying
    a. Nervous: (Enterogastric Reflex):increase irritation and acidity, decrease emptying

b. Hormonal: presence of fat in duodenum –>releases (CCK, GIP and secretin)

  1. Consistency of food: Liquid food is evacuated more rapidly > solids
  2. Reflexes from outside the GIT: Pain—>emptying
44
Q

Give the causes, center and mechanism of vomiting

A

Causes of vomiting:
x Reflex:
a. Mechanical stimulation of the posterior part of the tongue.
b. Irritation of the gastric mucosa
c. Irritation or obstruction of the intestine

Central: stimulate vomiting center
A- Drugs: apomorphine
B- Hypoxia and acidosis
C- Motion sickness

  1. Stomach wall is completely passive:
  • Relaxation of the wall of the stomach.
  • Relaxation of LES.
  • Contraction of pyloric sphincter
  1. Deep inspiration followed by contraction of abdominal muscles–> increase intra-abdominal pressure —> squeeze gastric contents up through a relaxed LES

Vomiting centers in medulla which is associated with respiratory center

45
Q

Give an account on defecation spinal reflex?

A

Stimulus: rectal distention

Afferent: pelvic nerve

Receptors: sensory nerve endings in the rectum

Center: sacral segments of spinal cord

Efferent: reflex back in pelvic nerves

response: contraction of smooth muscle distal colon and relaxation of internal anal sphincter

46
Q

Describe the mechanism of salivary secretion

A

First stage: acini secrete 1ry secretion, has ionic composition, 1ry secretion is isotonic

Secondary stage: ducts modify primary secretion, Na is reabsorbed in exchange with K. This decrease Na, Cl in saliva, while increase K, HCO3 in plasma. 2nd secretion is hypotonic

47
Q

Explain control of salivary secretion

A

Parasympathetic: center is in superior and inferior salivary nucleus: superior for sublingual and inferior for parotid gland. It causes marked VD which profuse secretion of watery saliva

Secretion of saliva:
Stimulus: taste, tactile stimuli from mouth and upper intestine

Conditioned:
Stimulus: sight, smell, preparation of food

48
Q

Mechanism of acid secretion

A
  1. H2O dissociates into H+ and OH- in the cell.
  2. H+ is actively secreted to lumen in exchange for K+ by H+/K+ ATPase pump
  3. CO2 (formed during metabolism or entering by blood and HCO3 is formed
  4. HCO3- diffuses out of the cell ї to blood in exchange for Cl-
  5. Cl- is actively transported to the lumen
  6. H2O passes to the lumen by osmosis.
49
Q

List Stimuli of HCL secretion & their mechanism of action, functions of HCL

A

Histamine: acts on H2 receptor increase cAMP
Ach: acts on M3 receptors, increase intracellular Ca
Gastrin: acts directly by increase Ca intracellular

50
Q

Describe the 3 phases of gastric secretion

A
  1. Cephalic stimulatory phase: (Nervous)—> 1/3 of gastric secretion
    x Both conditioned and unconditioned reflexes –> stimulate vagus—> increase gastric secretion by:
    a. Acetylcholine–>acts directly on parietal cells.
    b. Gastrin-releasing peptide–> increase gastrin secretion.
  2. Gastric stimulatory phase: (Nervous and Hormonal)–>2/3 gastric secretion): via
    a. Long vago-vagal reflexes
    b. Local enteric reflexes (submucous plexus)
    c. Gastrin secretion.
  3. Intestinal inhibitory phase: (Nervous and Hormonal)–> decrease gastric secretion by:
    A. Enterogastric reflex.
    B. Hormones inhibit gastric secretion, such as GIF, VIP, CCK and secretin.
51
Q

Mention the control of peristalsis of SI

A

Nervous regulation by gastroenteric reflex: initiated by distention of stomach –> conducted via myenteric plexus from stomach along SI

Hormonal regulation: gastrin, CCK, insulin, motilin and serotonin

52
Q

list Mechanisms of inhibition of gastric secretion?

A
  1. decrease pH< 2 in pyloric region & duodenum–> decrease gastrin
  2. Enterogastric reflex
  3. Presence of fat and hypertonic sugars in duodenum–> increase GIP, CCK, secretin and VIP.
  4. Emotional depression and fear, via impulses from cerebral cortex–> inhibit dorsal vagal nucleus.
  5. Somatostatin (paracrine).
53
Q

Describe the mucosal barrier? formed of

A
  1. Insoluble mucus (glycoproteins = mucins): secreted by surface mucous cells —> flexible coating gel
  2. HCI secreted by parietal cells in gastric glands crosses this barrier in finger like channels,
  3. Integrity of the membrane of mucosal cells:
    o Membrane is impermeable to H+
    o Active transport —> pumping H+ from mucosal cell into lumen, and Na+ from the cells into ISF.
  4. Prostaglandins
    o Strengthen and augment gastric mucosal barrier
    o inhibit acid secretion
54
Q

Discuss role of liver in controlling appetite?

A

јsugar levels їј FGF21 secretion from liverї signals to PVN in hypothalamus ї љ,K
ŝŶƚĂŬĞїљsweet-seeking behavior and meal size.
- FGF21: also ј insulin sensitivity & modulation of hepatic fatty acid oxidation and ketogenesis

55
Q

Discuss regulation of pancreatic secretion

A

During cephalic & gastric phases of gastric secretion —> increase parasympathetic vagal discharge—> release acetylcholine—> activating phospholipase C in pancreatic acinar cells —> secretion of small amount of pancreatic juice rich in enzymes.

56
Q

Discuss the hormonal function and immunological functions of liver

A

Hormonal functions:
Secretes IGF-1 which is involved in growth as well as angiotensinogen.

Immunity: liver is rich in cells of immune system like NK cells and Kupffer cells which secrete cytokines and activates immune system.

57
Q
A

DIG 209 FINAL (4 decks)

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