23/05 Flashcards

1
Q

what does omeprazole act on

A

Parietal cells are located in the epithelium lining the fundus and body of the stomach, and secrete HCl into the stomach using the H+/K+-ATPase pump. Omeprazole is a proton pump inhibitor (PPI) and therefore inhibits the H+/K+-ATPase pump.

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2
Q

2 primary bile acids

A

Cholic acid

Chenodeoxycholic acid

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3
Q

bile salts

A

cholic acid
Chenodeoxycholic acid
When these bile acids are conjugated with amino acids they form bile salts.

Bile salts are amphipathic which means they have a hydrophobic end (which is lipid soluble) and a hydrophilic end (which is water soluble).
This structure allows bile salts to emulsify fats which allows pancreatic lipase digest fats.

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4
Q

hepatotoxic drug eg

A

Amiodarone is a hepatotoxic drug. This means it is likely to cause damage to the hepatocytes and impair its ability to conjugate bilirubin, leading to hepatic jaundice.

used for bad ventricular tachy

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5
Q

Metoclopramide

A

Metoclopramide is a dopamine-receptor antagonist which causes relaxation of the lower oesophageal sphincter and increases gastric motility, leading to increased gastric emptying. Patients on these drugs may experience an increased appetite

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6
Q

Enterogastric reflex

A

The enterogastric reflex is stimulated by distension of the small intestine by the presence of chyme. Inhibitory signals are sent to the stomach via the enteric nervous system as well as signals to the medulla. Vagal stimulation of the stomach is reduced and gastric acid secretion is reduced.

feedback mechanism to regulate the rate at which partially digested food (chyme) leaves the stomach and enters the small intestine.

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7
Q

Brunner’s gland

A

Submucosa of the duodenum only

Brunner’s gland provide abundant alkaline mucous to neutralise the chyme entering from the stomach.

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8
Q

Gastric Inhibitory Peptide

A

Gastric Inhibitory Peptide (GIP) mediates the ileal brake reflex. This delays gastric emptying to prevent unabsorbed nutrients entering the lower ileum, and is mainly triggered by high levels of fat. The aim of the ileal brake reflex is to slow small intestine bolus transit, to increase absorption in the small intestine. If GIP is disrupted, this will therefore exacerbate malabsorption by interrupting this reflex.

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9
Q

What is mainly responsible for gastric-inhibitory peptide (GIP) secretion?

A

GIP belongs to a family of metabolic hormones called incretins. Incretins are released after eating a meal containing glucose. They cause beta cells of the pancreatic islets to release insulin and lower blood glucose levels.

excess insulin production and secretion continues after the glucose derived from the meal has been digested, causing the amount of glucose in the bloodstream to fall to a lower-than-normal level.

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10
Q

what does CCK do

A

Chole = “bile”, cysto = “sac”, kinin = “move” –> move the bile-sac (gallbladder).

The presence of fatty acids in chyme that passes through the duodenum stimulates gallbladder contraction and release of stored bile into the duodenum via CCK. Bile plays a key role in digestion of fat in the duodenum.

§

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11
Q

Frank-Starling curve of the heart shows

A

Stroke Volume and Preload

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12
Q

reason for oedema in heart failure?

A

Aldosterone promotes sodium and anion reabsorption, which increases the osmolality of the extracellular fluid. Thus, osmoreceptors in the hypothalamus detect this increase and stimulate ADH secretion, which acts to increase fluid retention and oedema.

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13
Q

Venous return =

A

(Mean systemic filling pressure - Right atrial pressure) / Resistance to venous return.

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14
Q

Muscarinic receptors

A

G-protein coupled receptors. (M1-M5)

M1 is excitatory and found in neural tissue, gastric parietal cells and salivary glands.

M2 is inhibitory and found in cardiac tissue.

M3 is excitatory and is principally found in exocrine and smooth muscle tissue.

Muscarinic receptors are involved in parasympathetic neural pathways, as well as sympathetic stimulation of the sweat glands. They are usually stimulated by acetylcholine (although they can be stimulated by muscarine) and they are inhibited by atropine.

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15
Q

Adrenoceptors

A

G-protein coupled receptors. sympathetic nervous system

Alpha1, Alpha2, Beta1 and Beta2.

Alpha1 (located in blood vessels and when stimulated cause vasoconstriction),

Beta1 (located in the heart and when stimulated cause increased heart rate and contractility)

Beta2 (located in the lungs and when stimulated cause bronchodilatation).

They are stimulated by adrenaline (typically acts on Beta adrenoceptors) and noradrenaline (typically acts on Alpha adrenoceptors).

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16
Q

Reactive hyperaemia

A

Reactive hyperaemia describes the vasodilatation and transient increase in blood flow that occurs in response to tissue ischaemia, as occurs in coronary thrombosis. This means that the level of blood flow after vessel occlusion is greater than the level of blood flow prior to the occlusion.

17
Q

elastic lamina found (perhaps counterintuitively) in muscular arteries only

A

of which there is an external and external component.

not in arteries , just elastin

18
Q

A 35 year old patient, who has had asthma for many years, is told that his condition causes some of his alveoli to receive less air than usual.

Which mechanism is the most effective means to correct this V/Q mismatch?

A

n order to maximise gas exchange, blood is redirected towards regions where there is sufficient ventilation. This allows for gas exchange to be at its most efficient and thus maintain a proper V/Q ratio

vasoconstriction

19
Q

Pneumothorax and compliance

A

one-way valve is created in which air can enter the pleural cavity but is unable to leave. This results in the progressive accumulation of air in the pleural cavity. The intrapleural pressure becomes greater than the atmospheric pressure, compressing the ipsilateral lung and reducing its compliance. As a result, the lung collapses and is unable to expand due to the pressure.

20
Q

pathophysiology of cystic fibrosis?

A

Cystic fibrosis transmembrane conductance regulator (CFTR) protein is important in the reabsorption of chloride and sodium ions across the surface epithelium. In the sweat glands, loss of CFTR protein causes impaired reabsorption of chloride and sodium ions, resulting in the production of hypertonic sweat.

30%

21
Q

residual volume

A

olume of remaining air after a maximal exhalation

22
Q

How does the calcium-sensing receptor (CaSR) found in the parathyroid gland’s chief cells respond to raised calcium levels?

A

By inhibiting the release of Parathyroid Hormone (PTH)

23
Q

Pre-hepatic jaundice

A

Due to excessive erythrocyte/RBC breakdown, the liver receives too much unconjugated bilirubin and cannot conjugate it all. The liver can only conjugated so much bilirubin until it becomes overwhelmed and the rest seeps into the bloodstream. Unconjugated bilirubin elevated

24
Q

hepatic jaundice

A

The actual liver is impaired in a way that its hepatocytes cannot conjugate bilirubin OR there is too much pressure within the liver and conjugated bilirubin becomes trapped within the intra-hepatic ducts. Both conjugated and unconjugated bilirubin elevated

25
Q

post hepatic jaundice

A

The pathway of bilirubin within the biliary tree is obstructed. This means conjugated bilirubin is stuck within the biliary tree and its pathway to the GI tract is blocked. This causes conjugated bilirubin to seep into the bloodstream. Conjugated bilirubin elevated

26
Q

cardiac cycle inflow/ filling phase

A

ventricles are filled with blood during diastole (heart relaxation) and atrial systole (atrial contraction). Blood enters the right atrium via the vena cava and enters the left atrium via the pulmonary vein. During diastole, the atrioventricular valves (mitral/tricuspid valves) are open and blood flows passively from the atria to the ventricles. This allows the ventricles to fill with blood at a steadily decreasing rate. The heart is mostly supplied with oxygenated blood during diastole as well. During atrial systole, the atria contract to force any remaining blood from the atria into the ventricles, further increasing ventricular pressure. When the pressure in the ventricles exceeds the pressure in the atria, it triggers the atrioventricular valves to close, resulting in the first heart sound (S1).

27
Q

cardiac cycle isovolumetric Contraction

A

start of ventricular systole. Both ventricles contract simultaneously which causes the ventricular pressure to increase. The atrioventricular valves and semi-lunar valves remain closed. This phase lasts roughly 50ms and is termed “isovolumetric” as there is no change in blood volume - only the ventricular pressure is changing. The carotid/radial pulse corresponds with ventricular systole.

28
Q

cardiac cycle Outflow (Ejection Phase)

A

ventricular pressure exceeds the pressure in the aorta/pulmonary artery, it triggers the semi-lunar valves (aortic valve/pulmonary valve) to open. Consequently, deoxygenated blood is ejected from the right ventricle into the pulmonary artery (to supply the lungs) and oxygenated blood is ejected from the left ventricle into the aorta (to supply the rest of the body). The atrioventricular valves remain closed during this phase to prevent backflow of blood from the ventricles to the atria. This phase lasts approximately 330ms.

29
Q

Isovolumetric Relaxation

A

At the end of the outflow phase, the ventricles relax and the pressure in the aorta/pulmonary artery once again exceeds the ventricular pressure. This pressure difference causes the semi-lunar valves to close, resulting in the second heart sound (S2). The atrioventricular valves also remain closed during this phase. The atria then begin to fill with blood again and the cycle repeats itself.