workshop 2 Flashcards
Explain how primary hyperaldosteronism leads to high blood pressure (2 marks).
What changes would you expect to see in Ms K’s blood electrolytes (1 mark)?
Explain how primary hyperaldosteronism leads to high blood pressure (2 marks).
- Primary hyperaldosteronism leads to high blood pressure through the overstimulation of the Renin-Angiotensin-Aldosterone System (RAAS). This condition causes the adrenal glands to secrete excessive amounts of aldosterone, which promotes:
* Increased Sodium Retention: Aldosterone stimulates the kidney to reabsorb more sodium from the distal convoluted tubules and collecting ducts. Resulting in the sodium retention leading to increased blood volume as water follows sodium osmotically, resulting in increased blood pressure.
* Vasoconstriction via Angiotensin II: Aldosterone release also increases levels of angiotensin II, which acts as a powerful vasoconstrictor. Raising peripheral resistance by constricting blood vessels, further contributing to increase in blood pressure.
What changes would you expect to see in Ms K’s blood electrolytes (1 mark)?
- From excess aldosterone from the primary hyperaldosteronism, Ms. K would likely experience increased sodium reabsorption and potassium excretion by the kidneys.
Explain how an ACE inhibitor would be effective as an antihypertensive (3 marks).
- ACE inhibitors work by blocking the conversion of angiotensin I into angiotensin II.
- Since angiotensin II is a potent vasoconstrictor, reducing its levels helps prevent blood vessel constriction.
-This reduction in vasoconstriction lowers peripheral resistance and subsequently decreases blood pressure
. Additionally, lower levels of angiotensin II would lead to less aldosterone release, reducing sodium and water retention, further lowering blood pressure.
Explain how loop diuretics would affect urine output (2 marks).
- Inhibition of Reabsorption: Loop diuretics act on the ascending limb of the loop of Henle, inhibiting the reabsorption of sodium, potassium, and chloride, which decreases water reabsorption and increases urine output.
- Electrolyte Imbalance: By preventing sodium and chloride reabsorption, loop diuretics lead to increased excretion of these electrolytes, potentially causing imbalances in the body’s electrolyte levels.
List and describe the three pressures operating at the filtration membrane and explain how each influences net filtration pressure (6 marks).
- Glomerular Blood Hydrostatic Pressure (GBHP) (2 marks)
- Description: This is the pressure exerted by the blood inside the glomerular capillaries. It is typically around 55 mm Hg.
- Influence on NFP: GBHP pushes water and solutes out of the glomerulus and through the filtration membrane into Bowman’s capsule, favoring filtration. It is the main driving force that promotes filtration.
- Capsular Hydrostatic Pressure (CHP) (2 marks)
- Description: This pressure, typically around 15 mm Hg, is exerted by the fluid already present in the capsular space against the filtration membrane.
- Influence on NFP: CHP opposes filtration by exerting back pressure, resisting the movement of new filtrate from the glomerular capillaries into the capsule.
- Blood Colloid Osmotic Pressure (BCOP) (2 marks)
- Description: BCOP, which is typically 30 mm Hg, is caused by plasma proteins in the blood that cannot pass through the filtration membrane.
- Influence on NFP: It draws water back into the capillaries by osmotic force, opposing filtration and reducing the amount of fluid that moves into Bowman’s capsule.
What effect will Farouk’s severe diarrhea have on net filtration pressure (2 marks)?
Farouk’s severe diarrhea leads to dehydration, which causes a reduction in blood volume. This results in a decrease in Glomerular Blood Hydrostatic Pressure (GBHP), while Blood Colloid Osmotic Pressure (BCOP) may increase due to higher plasma protein concentration in the reduced plasma volume. These changes decrease the Net Filtration Pressure (NFP), reducing the rate of glomerular filtration and consequently impairing kidney function.
Describe the digestive function of the gallbladder including its stimulatory regulation (4 marks).
- Digestive Function: The gallbladder stores and concentrates bile, which is produced by the liver. During digestion, the gallbladder releases bile into the small intestine.
- Stimulatory Regulation: When fatty food enters the duodenum, the hormone cholecystokinin (CCK) is released, stimulating the gallbladder to contract and release bile. Bile is essential for the emulsification of fats, breaking down large lipid globules into smaller droplets to aid fat digestion and absorption
Explain why digestion is minimally compromised following a cholecystectomy and why Sally might be experiencing episodes of diarrhea (4 marks).
- Digestion After Cholecystectomy: After the removal of the gallbladder (cholecystectomy), bile is still produced by the liver but is continuously secreted into the small intestine rather than being stored. This means there may be less bile available in response to a fatty meal, but overall fat digestion is still possible, although slightly less efficient.
- Diarrhea: Sally’s diarrhea could be due to the continuous flow of bile into the intestines without the gallbladder regulating its release. This can lead to irritation of the intestines and more rapid movement of contents through the digestive tract, resulting in diarrhea, especially after consuming fatty meals
Outline how triglycerides are digested and how they and their constituents are absorbed in the human body (8 marks).
Digestion (2 Marks)
- Enzymes: Digestion starts with lingual lipase in the mouth, continues with gastric lipase in the stomach, and primarily occurs in the small intestine with pancreatic lipase.
- Emulsification: Bile salts from the gallbladder emulsify large lipid globules into smaller ones, enabling efficient digestion by pancreatic lipase
Absorption (3 Marks)
- Micelles: Formed by bile salts, they surround fatty acids and monoglycerides, ferrying them to the brush border of enterocytes.
- Diffusion: Fatty acids and monoglycerides diffuse into enterocytes, where they recombine to form triglycerides. These triglycerides are then assembled into chylomicrons, which are transported out of the cell via exocytosis
Entry to Bloodstream (3 Marks)
- Chylomicrons: Exit enterocytes via exocytosis, enter lacteals (lymphatic vessels), and are eventually transported to the bloodstream through the thoracic duct
How does the detrusor muscle and the internal urethral sphincter respond to increased firing of the parasympathetic fibers that innervate it (1 mark)?
Increased parasympathetic activity causes the detrusor muscle to contract and the internal urethral sphincter to relax, allowing urine to be expelled from the bladder.
What effect would a spinal cord injury that has damaged the sympathetic nerves at the L2–L5 region of the spinal cord have on the micturition reflex (3 marks)?
- The information provided focuses on the role of parasympathetic activation for bladder emptying. A spinal cord injury affecting sympathetic nerves at L2–L5 would disrupt sympathetic control, impairing the ability of the internal urethral sphincter to maintain continence and leading to potential urine leakage.
- Additionally, the storage phase could be affected, as sympathetic activity is important for keeping the bladder relaxed and maintaining sphincter tone, leading to uncontrolled detrusor contractions and increased risk of incontinence (reflexive emptying).
Choose One of the auto-regulatory mechanisms that likely contributes to the regulation of GFR, relative to a situation where the GFR is initially low (4 marks).
Answer:
* Chosen Mechanism: Angiotensin II-mediated Regulation.
* How It Regulates GFR: When GFR is initially low, the renin-angiotensin-aldosterone system (RAAS) is activated. Angiotensin II acts as a powerful vasoconstrictor, causing constriction of the efferent arteriole, which helps maintain pressure within the glomerulus and supports increasing the GFR.
* Additional Effect: Angiotensin II also reduces GFR by constricting the afferent arteriole under certain conditions, helping conserve water and salts.
* Outcome: These actions stabilize GFR and ensure adequate kidney function despite changes in blood pressure or volume.
Describe in general how each organ contributes to the digestion process (4 marks).
Answer:
1. Salivary Glands:
The salivary glands (parotid, submandibular, and sublingual) produce saliva, which contains salivary α-amylase begins the chemical digestion of carbohydrates by breaking down starch into smaller molecules in the mouth
2. Liver:
The liver produces bile, which is stored in the gallbladder. Bile contains bile salts that are essential for the emulsification of fats, breaking down large lipid globules into smaller ones to increase their surface area for enzyme activity
3. Gallbladder:
o The gallbladder stores and concentrates bile, releasing it into the small intestine during digestion to aid in the emulsification of fats, which is crucial for lipid digestion by pancreatic lipase
4. Pancreas:
o The pancreas secretes pancreatic juice, which contains pancreatic enzymes such as pancreatic lipase (for lipid digestion) and amylase (for carbohydrate digestion). It also secretes proteases like trypsin and chymotrypsin to continue the breakdown of proteins in the small intestin
Why is it necessary for the stomach contents to be so acidic (2 marks)?
The stomach’s high acidity (pH around 2) is necessary to denature proteins, which makes them more accessible to digestive enzymes like pepsin. The acidity also activates pepsinogen into pepsin, which begins the digestion of proteins.
How does the stomach protect itself from digestion (2 marks)?
- The stomach protects itself by secreting pepsinogen, an inactive form of pepsin that prevents digestion of the stomach lining until it is activated in the stomach lumen.
- Additionally, the stomach lining is coated with alkaline mucus, which forms a protective barrier against the acidic gastric juice, preventing self-digestion
