Physiology: Renal, Hepatic & GI Flashcards

Review renal, hepatic, and gastrointestinal physiology to understand metabolism, drug clearance, and perioperative fluid balance. (63 cards)

1
Q

What does pancreatic lipase do?

A

Converts triglycerides to free fatty acids and 2-monoglycerides with the help of colipase.

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2
Q

Which cells secrete gastric acid, gastrin, pepsinogen, and somatostatin in the stomach?

A
  • Gastric Acid: Parietal cells
  • Gastrin: G-cells
  • Pepsinogen: Chief cells
  • Somatostatin: D-cells
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3
Q

How much of the hepatic oxygen requirement and blood flow is supplied by the hepatic portal vein?

A

Hepatic portal vein supplies 75% of blood flow and 50% of oxygen.

The common hepatic artery is a branch of the coeliac trunk.

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4
Q

Describe the hepatic artery buffer response mechanism.

A
  • Compensatory mechanism where the hepatic artery vasodilates due to reduced portal venous flow.
  • Adenosine is secreted at a constant rate into the space of Mall.
  • Reduced portal flow leads to adenosine accumulation, causing vasodilation of the hepatic artery.
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5
Q

Which kidney cells respond to increased pCO₂ by upregulating acid secretion?

A

Alpha intercalated cells in the collecting duct.

Most H⁺ removal in urine occurs via the H⁺/K⁺ antiporter in the distal convoluted tubule.

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6
Q

List the parts of a nephron and the diuretics that act on each.

A
  • PCT: carbonic anhydrase inhibitors
  • Ascending limb: osmotic and loop diuretics
  • Early DCT: thiazide diuretics
  • DCT: potassium-sparing diuretics
  • Late DCT and Collecting Duct: aldosterone antagonists
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7
Q

What are the primary and secondary bile acids?

A
  • The primary bile acids in humans are cholic acid and chenodeoxycholic acid.
  • Secondary bile acids are formed within the colon from primary bile salts via the action of bacterial flora.

Examples of secondary bile include lithocholic acid and deoxycholic acid.

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8
Q

Outline the urea cycle.

A
  • Primary means of elimination of ammonia (mitochondria and cytosol of hepatocytes)
  • Ammonia is converted to carbamoyl phosphate by carbamoyl phosphate synthetase (rate-limiting)
  • Carbamoyl phosphate reacts with ornithine to form citrulline.
  • Citrulline is converted to urea.
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9
Q

What are the main differences between zone 1 and zone 3 of the hepatic acinus?

A
  • Zone 1 (peri‑portal): high O₂ and nutrients → energy‑intensive tasks: glycogenolysis, gluconeogenesis, β‑oxidation, cholesterol synthesis.
  • Zone 3 (centrilobular): low O₂, rich in CYP‑450 → drug and toxin biotransformation.
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10
Q

By what degree does renal blood flow increase in pregnancy?

A

50%

This leads to an increase in GFR meaning that a low creatinine is to be expected in pregnancy

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11
Q

How much bile is produced every day and where is most of it reabsorbed?

A

600 mL per day; 90% absorbed in the terminal ileum.

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12
Q

Describe the Cori cycle.

A
  • Excess lactate from the muscles is transported to the liver where it undergoes gluconeogenesis (spends 6 ATP).
  • Pyruvate is generated which can be used in the Kreb’s cycle, which can only occur under aerobic conditions.
  • New glucose is transported to the muscle where it is used for glycolysis or converted to glycogen and stored.
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13
Q

What is hepcidin?

A

Peptide hormone produced in the liver that inhibits iron absorption and transport by binding to ferroportin channels in the basolateral membrane of enterocytes.

It prevents iron leaving enterocytes and prevents iron release from macrophages

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14
Q

Outline the three phases of gastric acid secretion.

A
  • Cephalic (30%): Anticipation of food triggers vagal stimulation, increasing motility and gastric juice secretion, along with gastrin and histamine release.
  • Gastric (60%): Gastric distension activates mechanoreceptors, initiating a vagal reflex. Antral distension with peptides further stimulates gastrin release.
  • Intestinal (10%): Duodenal distension and presence of peptides/amino acids lead to more gastrin secretion. Increased acidity prompts secretin release from duodenal S cells, inhibiting gastrin release.
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15
Q

What are the two mechanisms of renal autoregulation in response to blood pressure changes?

A
  • Myogenic response: Afferent arteriolar smooth muscle contracts when stretched due to calcium influx via stretch-activated channels, maintaining constant blood flow.
  • Tubuloglomerular feedback (TGF): Increased Na⁺ at the macula densa triggers afferent arteriole constriction, reducing GFR in response to elevated tubular flow.
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16
Q

State the equation for urinary clearance.

A

CL = V x U / P

U = urinary creatinine concentration (mg/ml)
V = urine volume (ml/min)
P = plasma creatinine concentration (mg/ml)

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17
Q

What are the two types of nephron?

A
  • Cortical (85%): short loops of Henle in the outer renal cortex.
  • Juxtamedullary (15%): long loops of Henle extending into the medulla, affecting medullary hypertonicity.
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18
Q

What are the stimuli for renin release?

A
  • Beta-1 stimulation
  • Renal artery hypotension
  • Reduced Na⁺ delivery to distal renal tubules (sensed by macula densa)

Renin is released by juxtaglomerular cells.

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19
Q

What are the functions of angiotensin II?

A
  • Vasoconstriction
  • Increase renal Na absorption (via Na/H exchanger and Na channels in collecting ducts)
  • Aldosterone release
  • ADH release
  • Thirst centres
  • Enhanced sympathetic adrenergic function

ANP and BNP are an important counter-regulatory system

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20
Q

What are the functions of bile?

A
  • Emulsification of lipids
  • Absorption of fat-soluble vitamins
  • Excretion of bilirubin
  • Acid neutralisation
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21
Q

Which cells produce secretin and what is its function?

A

Produced by duodenal S cells in response to acidic chyme. It:

  • Stimulates pancreatic and biliary bicarbonate secretion to neutralize acid
  • Inhibits gastric acid secretion and gastric emptying.
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22
Q

Which cells produce cholecystokinin and what are its functions?

A

Produced by I cells in response to fats and proteins. It:

  • Stimulates gallbladder contraction
  • Stimulates pancreatic enzyme secretion
  • Slows gastric emptying
  • Promotes satiety
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23
Q

Which cells produce gastrin and what are its functions?

A

Produced by G cells in response to food, distension, and vagal stimulation. It:

  • Stimulates gastric acid secretion
  • Promotes growth of gastric mucosa
  • Increases gastric motility
  • Prepares stomach for digestion.
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24
Q

What is the pH of the stomach and small intestine?

A

Stomach: 3
Small Intestine: 8

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25
Which **neurotransmitters** are important in intestinal contractions?
Tachykinins Acetylcholine
26
Describe the production of **hydrochloric acid** by gastric parietal cells.
* H₂CO₃ dissociates into H⁺ and HCO₃⁻. **HCO₃⁻ exchanges for Cl⁻** on the basal side of parietal cells. * K⁺ and Cl⁻ diffuse into **canaliculi** on the luminal side. * H⁺ is **pumped into the lumen** via H⁺/K⁺ exchanger, increasing H⁺ and Cl⁻ concentration in the lumen.
27
List some **mediators** that stimulate gastric acid production.
* Histamine * Gastrin * Acetylcholine
28
Which cells within the **GI tract** are responsible for coordinating **peristalsis** in the GI tract?
Interstitial cells of Cajal ## Footnote They are specialised pacemaker cells in the gastrointestinal tract that generate and coordinate smooth muscle contractions by producing slow-wave electrical activity.
29
What must happen to **dietary iron** before absorption into circulation?
* Reduced from ferric form (Fe³⁺) to **ferrous form** (Fe²⁺) * This occurs via **DCytB** at the brush border * Enters the cell through **DMT1** and exits into blood via **ferroportin** * Converted back to Fe³⁺ by **hephaestin** and **caeruloplasmin** before binding to **transferrin**
30
What are the **triggers** for renin release?
* Decreased sodium delivery to the macula densa * Decreased renal perfusion pressure * Sympathetic stimulation acting via beta-1 adrenoreceptors.
31
State the equation for **hepatic clearance**.
Hepatic Clearance = Hepatic Blood Flow x Hepatic Extraction Ratio
32
What is the **histological unit** of the liver?
Lobule ## Footnote A hexagonal structure with portal triads at the apices and a central vein in the middle. **Acinus** is the functional unit.
33
Describe the **control of liver blood flow**.
* Myogenic response * Hepatic artery buffer response (constant adenosine secretion) * Sympathetic nervous system * Drugs (e.g., noradrenaline reduces flow) * General and spinal anaesthesia (reduces flow) ## Footnote Portal venous flow is passive and cannot be regulated.
34
Outline the **functions** of the **liver**.
* **Biotransformation**: e.g., drugs * **Synthesis**: clotting factors, plasma proteins * **Metabolism**: glycogenolysis, gluconeogenesis, cholesterol synthesis * **Digestive**: bile production * **Storage**: iron, fat-soluble vitamins
35
List the four main **gut hormones** and their actions.
* **Gastrin** (G cells): secretes gastric juices, increases motility, constricts LOS * **GIP** (K cells): increases insulin release, inhibits gastric juices, slows gastric emptying * **Secretin** (S cells): stimulates gallbladder and pancreatic enzymes, augments CCK * **CCK** (I cells): stimulates gallbladder contraction, stimulates pancreatic enzymes, promotes satiety, inhibits gastric emptying
36
What is **oesophageal barrier pressure**?
The **difference in pressure** between the **LOS** (15-25 mm Hg) and **intragastric** pressure.
37
List some complications associated with **TPN**.
* Volume overload * Glucose abnormalities * Electrolyte abnormalities * Hepatic dysfunction * Refeeding syndrome
38
Describe **urinary buffering** of acids.
* In the PCT, **H⁺ is secreted in exchange for Na⁺** and combines with filtered HCO₃⁻ to form **carbonic acid**. * This dissociates to H₂O and CO₂, which enter the tubular cell, reversing the reaction to **generate HCO₃⁻ for reabsorption**. * H⁺ combines with NH₃ to form **NH₄⁺**, which is **excreted in urine**.
39
Why does **renal failure** lead to **acidosis**?
* Reduced tubular excretion of H⁺ * Excess K⁺ causes acidosis * Decreased bicarbonate generation * Reduced hemoglobin * Plasma protein loss from proteinuria
40
Describe the **control** of renal blood flow.
* Myogenic theory * Tubuloglomerular feedback * Renal sympathetic innervation * Angiotensin II * Renal prostaglandins
41
Describe the **tubuloglomerular feedback** mechanism.
* **Sensory**: Macula densa detects fluid delivery in the tubule. Signal transmitted to glomerulus. * **Effector**: Vascular smooth muscle adjusts GFR via vasodilation or constriction. Influenced by prostaglandins, thromboxane, NO, and endothelin.
42
How is **renal blood flow** measured?
Using plasma clearance of **para-aminohippuric acid (PAH)**: * PAH has a high extraction ratio (almost fully removed by kidneys). * A-V concentration difference equals renal arteriolar concentration. * Clearance of PAH = Urine [PAH] × urine flow / plasma [PAH]. * This calculates renal plasma flow, which can be converted to renal blood flow by adjusting for hematocrit.
43
What is **filtration fraction**?
Ratio of GFR to renal plasma flow (normally around 20%)
44
How can **GFR** be measured?
* Using the **clearance** of a suitable substance (e.g. inulin clearance) * Serum **creatinine** level (Cockcroft-Gault and MDRD)
45
What are the features of an **ideal substance** used to measure **glomerular filtration**?
* Freely filtered at glomerulus * Not reabsorbed or secreted * Not metabolised * No effect on filtration rate * Not toxic * Easy to measure in plasma and urine
46
What are the **Starling** forces acting at the **glomerulus**?
The forces include **hydrostatic pressure** in the glomerular capillaries and **osmotic pressure** from the blood plasma. ## Footnote These forces determine the net filtration pressure, influencing the rate of glomerular filtration.
47
How much **glucose** can be reabsorbed by the kidneys?
Glucose reabsorption is **proportional to the amount filtered** up to the transport maximum (**10 mmol/L** of venous glucose). ## Footnote Beyond this threshold, glucose appears in the urine.
48
What percentage of **cardiac output** goes to the liver?
25% (1500 mL/min)
49
What determines the **selectivity** of the **glomerular filtration barrier**?
* Pore size (< 7 kDa freely filtered, >70 kDa cannot pass) * Charge (negative charges repelled) * Plasma protein binding
50
Which **substances** are absorbed from the filtrate by the **proximal convoluted tubule**?
* 65% of **Na, K and water** * 90% **bicarbonate** * 85% **phosphate** (regulated by PTH) * 50% of **urea** * 100% **glucose and amino acids**
51
Give examples of **drugs** that are **actively secreted** into the tubule.
* Penicillin * Uric acid * Aspirin * Creatinine * Morphine
52
Which **aquaporin** responds to vasopressin and increases water reabsorption in the collecting duct?
AQP2 ## Footnote Stimulated by V2 (Gs protein)
53
What substances are secreted by the **stomach**?
* Hydrochloric acid (stimulated by H2, parasympathetic and gastrin) * Pepsinogen * Gastrin * Intrinsic factor * Mucus
54
How do **parietal cells** produce stomach acid?
CO₂ diffuses into the cell, reacts with water via **carbonic anhydrase** to form H⁺ and HCO₃⁻. **H⁺ is exchanged for K⁺** on the apical surface (H⁺/K⁺ ATPase), and **HCO₃⁻ is exchanged for Cl⁻** at the basolateral surface. Cl⁻ then diffuses into the stomach lumen. ## Footnote These cells have M3 and H₂ receptors.
55
What factors affect the rate of **gastric emptying**?
* Chyme (liquids pass through faster, high volumes promote emptying, proteins pass fastest then carbs then fat) * Acidity in duodenum stimulates secretin (impaired emptying) * Fat in duodenum (CCK slows emptying) * Sympathetic activation slows emptying * Disease states (e.g. gastroparesis in diabetes, drugs)
56
How long does **gastric emptying** take?
* Solids: Minimal emptying for **first 30 mins** (then linear emptying). * Liquids: Stomach volume shows **exponential decline**.
57
How do **neonatal kidneys** differ from adult kidneys?
* **Poor sodium handling**: risk of salt-wasting or hypernatremia. * **Delicate fluid balance**: immature concentrating ability increases risk of dehydration and fluid overload. * **Drug clearance**: lower GFR leads to prolonged half-life of renally excreted drugs.
58
Which transporters mediate **glucose reabsorption** in the kidneys?
* **Apical**: SGLT2 (90%) and SGLT1 (10%) in the PCT * **Basolateral**: GLUT2 and GLUT1 (from cells to blood)
59
What effect does an **increase in pCO₂** have on the kidneys?
* Increases H⁺ secretion (via Na/H exchangers and H⁺-ATPase) * Enhances bicarbonate reabsorption * Boosts ammonium excretion
60
What is a **sieving coefficient**?
* The sieving coefficient provides a **measure of how different molecules** move across a **semi-permeable membrane**. * In **renal replacement therapy**, it is the ratio of the concentration of a molecule in the ultrafiltrate compared to the concentration in the blood.
61
How long do glycogen, protein and fat stores last in starvation?
**Glycogen**: 24-48 hours **Protein**: 12 days **Fat**: 25 days
62
What is the main **buffering system** in the kidneys?
**Ammonia (NH₃)** combines with H⁺ in tubular cells to form ammonium ions (NH₄⁺), which are excreted in urine to remove 30-40 mmol of H⁺ daily. ## Footnote Dihydrogen phosphate (HPO₄²⁻ + H⁺ → H₂PO₄⁻) is another important urinary buffer for H⁺ excretion.
63
Where does the **ammonia** come from in the kidneys?
Glutamine metabolism