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Year 2 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What is Wilson’s disease?

A

A disease that causes copper to build up in the body, can cause liver disease

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2
Q

What are some cholestatic symptoms?

A

Pruritis, pale stools, dark urine

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3
Q

What would the INR be in liver disease?

A

High as decreased production of coagulation factors

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4
Q

What fo ALT above 500 and above 1500 suggest?

A

above 500 - autoimmune condition, above 1500 suggests hepatitis, drugs and ischemia

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5
Q

Deficiency of what can lead to Werninke’s encephalopathy?

A

Thiamine (B1)

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6
Q

How do you treat oesophageal varices?

A

Resus patient, Terlipressen which dilates splanchnic vessels, antibiotics

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7
Q

What’s the difference between NASH and NAFLD?

A

NASH is a more serious form of NAFLD where liver has now become inflammed (Mallory-Denk bodies on histology slide)

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8
Q

How is NAD+ and NADH related to alcohol?

A

During ethanol oxidation mediated by ADH, NAD+ is converted to NADH and higher NADH levels tells the cells to make more fatty acids (less fatty acid oxidation)

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9
Q

What level does the coeliac trunk branch at?

A

T12

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10
Q

What level do superior and inferior mesenteric arteries branch from?

A

L1 and L3

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11
Q

What is a positive Murphy’s sign?

A

Indicative of cholecystitis - palpate under costal margin, ask patient to inhale and if gallbladder inflammed it will cause pain

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12
Q

Where do direct inguinal hernias occur in relation in inferior epigastric vessels?

A

Medially

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13
Q

What is patent in indirect hernias?

A

Processus vaginalis

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14
Q

What innervates the external anal sphincter?

A

Pudendal nerve

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15
Q

Why do you get refeeding syndrom?

A

Metabolism changes from FAs to carbs, causes insulin secretion and ions to return to cells at expense of plasma concentration

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16
Q

How does acidaemia effect potassium levels?

A

Leads to hyperkalaemia as tissues release K+ in exchange for H+ from the blood

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17
Q

What causes low gap acidosis?

A

Drop in albumin - as albumin is the major unmeasured anion

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18
Q

How does glucose enter beta cells?

A

Via GLUT2 transporter

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19
Q

What is glucagon inhibited by?

A

Hyperglycaemia, GLP1, somatostatin, insulin, zinc

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20
Q

What inhibits growth hormone release?

A

Somatostatin

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21
Q

What stimulates growth hormone release?

A

Ghrelin, androgens, leptin, nutrition, exercise

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22
Q

Options for treating severe hypoglycaemia?

A

IV dextrose and intramuscular glucagon

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23
Q

How do biguanides eg metformin work?

A

they decrease liver production of glucose (gluconeogenesis) and enhance insulin sensitivity

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24
Q

What is a side effect of biguanides that mean it is contraindicated in patients with HF, liver and renal disease?

A

Lactic acidosis

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25
Q

How do thiazolidinediones work? Eg pioglitazone

A

increases the activity of PPAR-y, which promotes triglyceride storage in adipose tissue

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26
Q

How do sulfonylureas work?

A

They stimulate insulin release from the pancreas by binding to sulfonylura receptor -therefore only work when some beta cell activity (They may induce hypoglycaemia)

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27
Q

What type of drug is exenatide and tirzepatide?

A

GLP-1 agonist. Promotes insulin secretion, inhibits glucagon prod and prolongs gastic emptying

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28
Q

What type of drugs are empagliflozin and dapagliflozin?

A

They are sodium-glucose cotransporter inhibitors for diabetes, increase urinary glucose excretion

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29
Q

When might you see Kussmaul respiration?

A

In diabetic ketoacidosis - deep laboured breathing - body trying to remove carbon dioxide (an acid)

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30
Q

What is diabetic nephropathy characterised by?

A

Proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis

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31
Q

What does glycation of apolipoprotin do?

A

Impairs cholesterol efflux from atherosclerotic plaques

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32
Q

Where is the vomiting centre located?

A

Within the lateral reticular formation of medulla oblongata

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33
Q

What class of drugs are cyclizine, dramaine and dimenhydrinate?

A

antihistamine - H1 antagonist

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34
Q

What class of drug is aprepitant? for sickness

A

NK-1 receptor antagonist

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35
Q

What class of drugs are often used for postop nausea?

A

5HT3 receptor antagonists

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36
Q

Where is cholecystokinin (CCK) synthesised?

A

L cells in duodenum in response to fat and protein

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37
Q

What does CCK do?

A

Slows gastric emptying, releases bile and pancreatic enzymes and induces satiety

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38
Q

How does leptin act as a satiety signal?

A

By inhibiting NPy/ AgRP neurones and activating POMC/CART neurones

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39
Q

How does oxyntomodulin impact appetite?

A

It decreases grelin

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40
Q

What does an increase in malonyl coA do?

A

It suppresses food intake. Acts on CPT1c receptors to stimulate POMC/CART neurones

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41
Q

What type of drug is orlistat?

A

Lipase inhibitor

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42
Q

What type of drug is wegovy (semaglutide)

A

GLP1 agonist

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43
Q

What are features of metabolic syndrome?

A

Insulin resistance, abdominal obesity, dyslipdaemia, hypertension

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44
Q

What enzyme is inhibited by steroids so they inhibit inflammation?

A

Phospholipase A2

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45
Q

How can B12 and folate deficiency be linked to CVD?

A

Results in low methionine levels and high blood homocysteine. Homocysteine is converted to toxic thiolactone which damages endothelial cells

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46
Q

Which part of adrenals is neural and which part glandular?

A

Medulla is neural - secretes adrenaline and noradrenaline
Cortex is glandular

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47
Q

What zone secretes cortisol?

A

Zona fasiculata

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48
Q

What does zona reticularis secrete?

A

Androgens

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49
Q

Where does superior suprarenal arteries branch from?

A

Inferior phrenic

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50
Q

What is the venous drainage of the adrenals?

A

Right suprarenal drains directly into IVC
left suprarenal drains directly into left renal vein which eventually drains into IVC

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51
Q

What are the four infrahyoid muscles that depress the hyoid bone?

A

Omohyoid, sternohyoid, sternothyroid, thyrohyoid

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52
Q

What is venous drainage of thyroid gland?

A

Superior and middle thyroid vein drain into IJV
inferior thyroid vein drains into brachiocephalic vein

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53
Q

What does damage to one and two recurrent laryngeal nerves do?

A

1= hoarse voice
2=dysphonia

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54
Q

Whereabouts would a gallstone have to be to cause pancreatitis?

A

Ampulla of Vater

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55
Q

What happens to calcium during alkalosis?

A

Ionised calcium falls as more of it binds to albumin to replace the lack of H+ ions. This leads to symptoms like tingling of the lips
Can cause sudden cardiac death

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56
Q

What does hypocalcaemia do?

A

It increaes permeability of excitable membranes to sodium which causes tachyarrythmias and tetany

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57
Q

In cardiac action potential what causes the plateau phase?

A

Calcium ions enter via L-type channels. Electrically balanced through K+ efflux

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58
Q

What is hyperkalemia effect on action potentials?

A

More excitability. More K+ outside cell leads to increased positivity, easier for sodium ions to enter which leads to depolarisation and increased risk of tachycardia

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59
Q

What stimulates the release of PTH?

A

Low serum calcium (and drops in Mg)

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60
Q

What cells secrete PTH?

A

Chief cells

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61
Q

What suppresses release of PTH?

A

Calcium binding to CaSR
Activated Vit D (calcitrol) suppresses PTH transcription
Also Cinacalet (a calcimimetic drugs used to treat hyperparathyroidsim)

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62
Q

What are the actions of PTH?

A

Kidney - decreases calcium excretion and increases phosphate excretion (kidney exception)
Bone - increases calcium and phosphate resorption
Inttesitne - increases calcium and phosphate resorption

OVERALL increases calcium, decreases phosphate

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63
Q

What cells are useful for nuclear medicine scanning of parathyroids?

A

Oxyphil cells - take up technetium sestamibi

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64
Q

Where does most resorption of calcium take place?

A

Proximal tubule (but it is PTH independent)

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65
Q

What effect do loop diuretics have on calcium?

A

Hypocalciaemia

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66
Q

Whereabouts in the kidney does PTH upregulate TRPV channels, calcium ATPase and Na/ca exchanger to leads to less calcium excretion?

A

Distal tubule

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67
Q

What do loop diuretics act on?

A

The Na/K/Cl co-transporter where they compete with Cl for the binding site

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68
Q

What do thiazides work on?

A

Na+/Cl- symporter in distal convoluted tubule

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69
Q

What does renal PTH do for vit d?

A

It activates it - Stimulation of 25(OH) D3 to 1,25(OH)2 D3 by upregulating 1-alpha hydroxylase

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70
Q

What do PTH and calcitriol stimulate in bone?

A

RANKL production (and downregulates OPG)

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71
Q

What can be given intermittently for osteoporosis but id given continuously will cause increased bone resorption?

A

PTH

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72
Q

What might you see on xray of someone with primary hyperparathyroidism?

A

Terminal tuft erosion, rugger jersey spine, brown tumours (not tumours - sites of bone remodelling)

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73
Q

Why can Tb and granulomatous conditions lead to hypercalcemia?

A

Bc the macrophages within the granulatomas have a positive feedback loop on the VitD receptors. So someone sunbathes, produces a lot of Vit D which then feeds back to increase calcium levels

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74
Q

What gene mutation can lead to Autosomal dominant hypophosphataemic rickets?

A

FGF23

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75
Q

What is FGF23 secreted by and what does it do?

A

By osteocytes and it reduces serum phosphate by decreasing its resorption in the kidneys

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76
Q

What is difference between primary and secondary hyperparathyroidism?

A

Primary caused by hyperplasia, adenomas, carcinomas of thyroid whereas secondary is a physiological compensation for hypocalcemia or vit D deficiency

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77
Q

What causes tertiary hyperparathyroidism?

A

happens after long-term secondary hyperparathyroidism when the parathyroid glands have been producing high levels of parathyroid hormone for such a long time that they become overgrown and permanently overactive

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78
Q

In familial hypocalciuric hypercalcemia what do the mutations affect?

A

Inactivating mutations of Calcium sensing receptor

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79
Q

What is the most potent stimulator of aldosterone?

A

Serum potassium levels

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80
Q

What effects does aldosterone have in kidney?

A

It increases Na+ and water reabsorption and decreases K+ secretion

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81
Q

What is Conn’s syndrome?

A

Primary hyperaldoesteronism

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82
Q

What are three mainstays of Conn’s

A

hypertension, hypokalemia, metabolic alkaosis

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83
Q

How would you treat bilateral Conn’s disease?

A

Mineralcorticoid receptor antagonists or potassium sparing diuretics

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84
Q

What is Liddle syndrome?

A

It is an autosomal dominant mutation in the ENaC sodium channel which leads to a high level of expression - hypertension, hypokalemia, metabolic alkalosis

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85
Q

What does the binding of ACTH to MC2R on receptor of ZF cells do?

A

It upregulates the enzymes involved in converting cholestrol to cortisol

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86
Q

What is Cushings an excess of?

A

Glucocorticoid - cortisol

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87
Q

What could an ectopic ACTH secreting neuroendocrine tumour cause?

A

Cushings syndrome

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88
Q

What can a high overnight dexamethasone suppression test be a sign of?

A

Cushing’s. Dexameth is a glucocortiod med and should provide neg feedback to pituatary to suppress ACTH production and in turn suppress cortisol

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89
Q

What is Addison’s disease?

A

Adrenal insufficiency - low cortisol and aldosterone

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90
Q

Why do you get hyperpigmentation in Addison’s disease?

A

ACTH stimulates the MC1R in the skin

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91
Q

What would you find in Addison’s disease?

A

Low BP, Low glucose, low Na, High K

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92
Q

How do you treat Addison’s disease?

A

Replacement steroids - hydrocortisone to replace glucocorticoid and fludrocortisone to replace mineralcorticoid

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93
Q

How do you diagnose Addison’s?

A

Low 9am cortisol
High ACTH
Short synACTHen Test

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94
Q

What are phaeochromocytomas?

A

Tumours of chromaffin cells in medulla

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95
Q

What is phenoxybenzamine?

A

An alpha blocker - given pre-operatively with beta blocker.
alpha blocker to stop the hypertension, beta blocker to stop the associated tachycarida

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96
Q

What does the 11 betaHSD-2 enzyme do?

A

Oxidises cortisol to the inactive cortisone to prevent activation of MCR

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97
Q

Name two mineralcorticoid receptor antagonists?

A

Spironolactone and eplerenone

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98
Q

Where does the thyroid descend from in development?

A

Foramen Cecum

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99
Q

Where is TRH secreted?

A

Paraventricular nucleus of the hypothalamus

100
Q

Where is TSH secreted?

A

By the thyrotropes in the anterior pituitary gland

101
Q

What form is 80% of thyroid hormone?

A

T4

102
Q

What is the inactive form of thyroid hormone?

A

T4

103
Q

What transports thyroid hormones around the blood?

A

Thyroxine binding globlin

104
Q

What happens to thyroid during pregnancy?

A

Increase of oestrogen causes sialyation of TBG which means it is cleared slower from plasma. Binds to more T4 which means less T4 is free for uptake by cells

105
Q

What are the functions of the three thyroid deiodinases?

A

D1 = plasma T3 production
D2= local t3 production
D3 = T3 degradation

106
Q

Which of the thyroid deiodinases are present in brain, placenta and foetus?

A

D3

107
Q

What thyroid deiodinases are upregulated in hypothyroidism

A

D2 (opposite for hyper)

108
Q

What heart problems common in hyperthyroidism?

A

Tachycardic and AF

109
Q

What effect does hyperthyroidism have on insulin?

A

Reduced insulin secretion and increased insulin turnover, leads to hyperglycaemia

110
Q

What disease do you get lid lag and lid retraction?

A

Hyperthyroidism/Graves

111
Q

Name a skin problem you get in hyperthyroidism?

A

Pretibial myoxedema

112
Q

What is Grave’s disease?

A

Autoantibodies that bind to THSR and cause over-expression of thyroid hormone

113
Q

Why do you get Grave’s eye disease?

A

Bc retrooribital fibrocytes express TSH receptor
Bind to this, T cells, lymphocytes release IFNy and fibroblasts secrete GAGS

114
Q

How would you treat a toxic adenoma?

A

Treat with I-131 radioactive iodine

115
Q

What drug can cause thyrotoxicosis?

A

Amiodarone - drug to treat arrythmias

116
Q

What is a struma ovarii?

A

a benign cystic teratoma containing majority thyroid tissue which can cause hyper thyroidism

117
Q

What are the two drugs for managing hyperthyroidism?

A

Propylthiouracil and carbimazole (both inhibit TPO)

118
Q

What waves are present on ECG in hypothermia

A

J waves (looks like a camel hump)

119
Q

Why might you find mild hyponatraemia in hypothyroidism?

A

Bc you have a reduced GFR

120
Q

How do you treat hypothyroidism?

A

Levothyroxine (T4)

121
Q

How can corticosteroids help with treatment of Hashimoto’s?

A

They decrease TBG (thyroxine binding globulin) which means more free T4

122
Q

In Hashimoto’s what are there antibodies against?

A

TPO which leads to follicular cell apoptosis

123
Q

How does Acetazolamide work?

A

It is a carbonic anhydrase inhibitor - blocks resorption of bicarbonate (in proximal convoluted tubule). Promotes bicarbb, sodium and chloride excretion

124
Q

What type of drugs are frusemide and bumetanide?

A

Loop diuretics

125
Q

What do loop diuretics act om?

A

Binds with chloride binding site on Na+/K+/2Cl- transporter

126
Q

What’s a side effect of loop diuretics?

A

Kidney stones bc more calcium in the urine

127
Q

What drugs are benfroflumethiazide and hydrochorothiazide?

A

Thiazide diuretics

128
Q

Where do thiazide diuretics work?

A

On the distal convoluted tubule. They block the sodium chloride co transporter

129
Q

What imbalance can thiazides cause?

A

Hypercalcaemia
Hyponatraemia
Hypokalemia

130
Q

What are the two classes of potassium sparing diuretics?

A

Epithelial Na channel antagonists and aldosterone antagonists

131
Q

When are aldosterone antagonists used?

A

Hyperaldosteronism, HF, hypokalaemia (from other diuretics)

132
Q

What stimulates IGF-1 production and where is it produced?

A

Growth Hormone and in the liver

133
Q

What inhibits growth hormone release?

A

somatostatin

134
Q

What effect does arginine vasopressin have on cortisol?

A

It stimulates ACTH which stimulates cortisol release

135
Q

What does ghrelin do to growth hormone?

A

Stimulates the release of it

136
Q

What mutation causes McCune-Albright syndrome?

A

GNAS gene
Not inherited (mosaic)

137
Q

What problems might you find with McCune-Albright?

A

Fibrous dysplasia
Cafe au lait spots
endocrine dysfunction - precocoious puberty

138
Q

What mutation can cause pituatary tumours?

A

AIP

139
Q

What gene can cause gigantism?

A

duplication or upregulation of GPR101

Giant
People
Rise
101

140
Q

What mutation causes red hair and fair skin?

A

MC1-R
(melanocortin 1 receptor)

141
Q

Cushing’s disease vs syndrome?

A

disease = when there is a pitutary tumour causing it
syndrome = group of symptoms you get when you have excess cortisol

142
Q

What does inhibin do?

A

Inhibits secretion of LH and FSH

143
Q

When might GnRH agonists be given?

A

In breast or prostate cancer. Continuous pituatary stimulation - receptor desensitisation stops from producing androgens

144
Q

What does kisspeptin stimulate?

A

Secretion of GnRH

145
Q

What is Kallmann syndrome

A

failure of correct production of GnRH - reproductive problems along with no sense of small. Comes from failure of development of olfactory neurons

146
Q

What is diabetes insipidus a deficiency of?

A

AVP (No insertion of aquaporins into membrane)

147
Q

How can you treat diabetes insipidus?

A

DDAVP = desmopressin

148
Q

Ratio of what carry a better diagnostic value of lipid associated CV risk that total cholestrol of HDL?

A

ApoB/ApoA ratio

Apo B carries Bad LDL
Apo A is ACE carries Good

149
Q

What does eGFR look at?

A

Creatine clearance from plasma

150
Q

What breast cancer antigens are used to monitor treatment?

A

CA15-3 and CA27-29

151
Q

What can be used to help diagnose liver cancer?

A

Alpha-fetoprotein

152
Q

What happens to mesonephric duct and paramesonephric in females?

A

Mesonephric duct degenerates and paramesonephric (Mullerian) forms oviduct

153
Q

What happens to mesonephric and paramesonephric duct in males?

A

Mesonephric forms male reproductive tract
paramesonephric degenerates

154
Q

What might you find in a pregnancy with a foetus with bilateral agenesis?

A

Oligohydramnios as in the uterus fetal kidney is important for generation of amniotic fluid

155
Q

What does a horse shoe kidney get stuck on

A

Inferior mesenteric artery

156
Q

What causes autosomal dominant and autosomal recessive polycystic kidney?

A

Autosomal dominant = problem with polycystin PKD-1 and PKD-2

Autosomal recessive: problem with fibrocystin

157
Q

What subunit do HCG, FSH, LH and TSH all share?

A

Alpha

158
Q

What substance is freely filtered by glomerulus and can be used to estimate GFR?

A

Creatinine

159
Q

Why does creatinine overestimate GFR?

A

It is actively secreted by peritubular capillaries

160
Q

What condition is characterised by a defect in the apical NaCl cotransporter at DCT lead to?

A

Gitelman’s. (Mimics effects of thiazides - hypokalaemia, hypomagnesia, hypercalcaemia)

161
Q

What does Bartter type 1 mimic the effects of?

A

Loop diuretics (Furosemide)

162
Q

What classes of diuretic act on proximal tubule?

A

Carbonic anhydrase inhibitors

163
Q

What diuretic is used in volume overload from CKD?

A

Loop diuretic

164
Q

What nerve inhibits sympathetic efferents to allow micturition to occur?

A

Hypogastric nerve

165
Q

What part of loop is impermeable to water?

A

Thick ascending loop, it is where active transport of sodium takes place

166
Q

In the presence of ADH what happens to aquaporins?

A

They become permeable to water allowing passage of water from collecting tubule to interstitium down a conc gradient

167
Q

What are Councilman bodies?

A

hepatocytes undergoing apoptosis

168
Q

What acts as a glucose sensor?

A

glucokinase

169
Q

What ratio leads to insulin secretion?

A

Increased ATP to ADP ratio, closes potassium channel = depolarisation. Opens calcium channel, triggering insulin secretion

170
Q

What stimulates insulin release besides glucose?

A

leucine and arginine (amino acids)
other things like glp1 and cck can potentiate but require glucose

171
Q

What are the catecholamines synthesised from and where?

A

phenylalanine and tyrosine in chromaffin cells of medulla

172
Q

What receptor do the catecholamines signal through?

A

G-protein coupled receptor

173
Q

Where is glucagon like peptide synthesised?

A

primarily in ileo-colonic (L) enteroendocrine cells

174
Q

What is a congenital problem of the foregut?

A

oesphageal atresia - oesophagus seals itself off

175
Q

What are three problems of mid gut?

A

1) duodenal atresia
2)meckel’s diverticulum - when yolk sak remnant persists
3) malrotation / volvulus

176
Q

What is Hirschprung disease?

A

a congenital megacolon due to lack of enteric neurones in distal part of gut

177
Q

What muscle supports the external anal spinchter and assists in creating anorectal angle?

A

Puborectalis

178
Q

What supplies motor supply to external anal spinchter?

A

inferior rectal nerve ( via pudendal )

179
Q

What is innervation of internal anal spinchter?

A

autonomic -
sympathetic from L5 segment via hypogastric plexus
parasympathetic from S2 to S4 via pelvic plexus

180
Q

what causes passive incontinence vs urge incontinence?

A

passive - problem with internal sphincter
urge - problem with external

181
Q

What creates the inguinal ligament?

A

inferior border of external oblique

182
Q

What abdominal muscle is absent in the inguinal canal?

A

transversus abdominis

183
Q

Nerve roots of genitofemoral reflex?

A

L1 L2
Cremaster cremaster L1 L2 pulls your balls up faster

184
Q

Where do you find the deep inguinal ring?

A

Mid point of inguinal ligament

185
Q

Which is raised more in liver damage due to alcohol?

A

AST>ALT

186
Q

What is the name of the pouch between the liver and the kidney?

A

Morrison’s pouch - hepato renal recess

187
Q

What are the oesophageal porto-systemic shunts between?

A

Left gastric vein, azygous

188
Q

What veins are involved in caput medusa?

A

enlarged epigastric veins and intercostal veins from recanalising of ligamentum teres

189
Q

What enzyme catalyses the breakdown of triglycerides into free fatty acids and glycerol?

A

Hormone sensitive lipase

190
Q

What happens to glucagon in diabetes?

A

excess circulating glucagon levels (as although there is a lot of glucose in blood, cant get into cells so they are still starving)

191
Q

How does pancreas initially respond to insulin resistance?

A

new beta cells are initially generated so islets increase in both size and number

192
Q

What is MODY and what is it caused by?

A

Maturity Onset diabetes of the young
Monogenic diabetes - mutation in one gene in autosomal dominant way

193
Q

What is the most common autoantibody in latent autoimmune diabetes of adults?

A

Gluatamic acid decarboxylase antibody

194
Q

What is Teplizumab for T1D a monoclonal antibody for?

A

Anti-CD3 antibody

195
Q

What are DPP-4 inhibitors/ when are they given?

A

DPP-4 degrades GLP1 so given with GLP1 agonists, by inhibiting GLP will stay for longer

196
Q

What part of the kidney do SGLT2 inhibitors work on?

A

The SGLT2 in renal proximal convoluted tubule

197
Q

What are flavonoids?

A

pigmented polyphenol plant compounds, found in fruit veg, tea and coffee. Beneficial for stroke and MI

198
Q

What can high levels of IGF-1 in the blood be a sign of?

A

acromegaly or growth hormone excess

199
Q

What does HbA1c measure?

A

glycated haemoglobin

200
Q

What requires peripheral de-iodination to achieve its maximal effect?

A

Thyroxine

201
Q

What is the name for t3?

A

triiodothyronine

202
Q

What does TPO do?

A

catalyzes the oxidation of the iodide to its active form, I2, and the binding of this active form to the tyrosine in thyroglobulin to form mono- or diiodotyrosine

203
Q

What is oxybutinin used for?

A

overactive bladder - it is an antimuscarinic blocking actions of acetyl choline

204
Q

What part of the kidney secretes aldosterone?

A

zona glomerulosa (it is a mineralcorticoid)

205
Q

What vitamin should be given to alcoholic cirrhosis patients to prevent wernike-korsakoff encephalopthy?

A

b1 - thiamine

206
Q

What lipoprotein main role is reverse cholestrol transport?

A

HDL

207
Q

what immune cells are involved in atherosclerosis and release cholestrol when they die?

A

macrophages

208
Q

What are the two substances secreted by posterior lobe?

A

ADH and oxytocin

209
Q

What are the endocrine functions of pancreas?

A

releases insulin and glucagon into blood stream

210
Q

What recieves sensory inputs for control of vomiting?

A

nucleus tractus solitarius

211
Q

What type of drugs are hyoscine / scolpalamine?

A

alkaloid and anticholinergic drugs on m3/m5

212
Q

What type of drugs are metoclopramide and domperidone? (nausea)

A

dopamine D2 receptor antagonists

213
Q

Why do chemo drugs cause sickness?

A

bc they liberate 5HT from enterochromaffin cells within mucosa of upper GI

214
Q

What do the 5Ht3 anti cancer sickness all end in?

A

-setron

215
Q

What atypical anytipsyhotic can be used in breakthrough vomiting?

A

Olanzapine

216
Q

What is the equation to work on pH?

A

pH = -log10 [H+]

217
Q
A
217
Q

Where does the majority of bicarbonate reabsorption take place?

A

proximal tubule

218
Q

Why do you get normal anion gap acidosis ?

A

occurs due to a primary loss in bicarbonate but you get a compensatory rise in chloride

219
Q

What accounts for greater than 90% of ases of hypercalcemia?

A

PHPT and malignancy

220
Q

What is the inactive form of cortisol?

A

cortisone

221
Q

What is saline suppression test?

A

test for Conn’s, give infusion of saline, see if aldosterone falls

222
Q

What receptor does ACTH bind to to cause the release of glucocorticoids?

A

MC2R (melanocortin receptor 2) / ACTH receptor

223
Q

What is glucocorticoid remediable aldosteronism?

A

is a heriditary form of primary hyperaldosteronism where aldosteron synthase becomes ACTH sensitive

224
Q

Where is CRH released?

A

hypothalamus, causes release of ACTH

225
Q

What are paragangliomas?

A

extra-adrenal chromaffin cell tumours

226
Q

What might you on see on ECG for hypothyroidism?

A

J waves of hypothermia
bradycardia

227
Q

If peripheral oedema up to sacrum how much weight do you need to take off to work out dry weight?

A

10kg
5kg if up to knee
1kg if just around ankle

228
Q

Where is ghrelin sectreted?

A

gastric fundus

229
Q

Where is glucose-dependent insulinotrophic polypeptide released?

A

by k cells in small intestine (anorexigenic hormone)

230
Q

why is leptin not a target for obesity?

A

Bc obese individuals have high leptin anyway and are said to have leptin resistance similar to db/db mouse

231
Q

Whereabouts in hypothalamus is food intake controlled?

A

arcuate nucleus

232
Q

What do AGRP/NPY neurones release which activates Y1 receptors to increase food intake?

A

NPY

233
Q

How do POMC/CART neurones decrease food intake?

A

By releasing melanocortins

234
Q

what are caveats about using creatinine for GFR ?

A

muscular people have high creatinine, malnourished low and some drugs inhibit secretion of creatinine

235
Q

What stimulates the release of ACTH?

A

Coritcotroph releasing hormone and arginine vasopressin

236
Q

What does oestrogen and testosterone feed back on on gonadal axis?

A

Feed back on KNDY cells which release kisspeptin triggering GnRH release

237
Q

What does metanephric kidney develop from?

A

mesonephric duct

238
Q

where do carbonic anhydrase inhibitors work?

A

proximal convulted tubule

239
Q

what acid base balance does acetazolamide cause?

A

metabolic acidosis (counteracts resp alkalosis)

240
Q

What do 5-alpha reductase inhibitors lead to less of in the blood?

A

DHT

241
Q

what type of drug is mirabegron? (urge incontinence)

A

Beta 3 adrenergic

242
Q

What cells are renin producing?

A

juxtaglomerular

243
Q

How can you distinguish the distal tubule from the proximal tubule?

A

a lack brush border and rich in mitochondria to provide energy for ion pumps

244
Q

What cells are regulators of acid base balance in the collecting ducts?

A

intercalated cells

245
Q

what do cortical vs medullary fibroblasts produce?

A

cortical produce erythropoietin
medullary produce gylcosamingolycans and prostaglandin E2

246
Q

What gene is involved in the majority of clear cell carcinomas?

A

VHL gene - Von Hippel Lindau disease

Year 2 (10 decks)

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