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Year 2 > Case 10 > Flashcards

Case 10 Flashcards

1
Q

Effect of Thyrotropin releasing hormone (TRH)

A

Thyroid stimulating hormone release from anterior pituitary

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2
Q

Proportion of anterior pituitary which secretes TSH

A

3-5%

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3
Q

Effect of GHRH

A

GH release from anterior pituitary

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4
Q

Effect of GnRH

A

Gonadotrophin release from anterior pituitary (LH and FSH)

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5
Q

Effect of corticotropin releasing hormone

A

ACTH release from anterior pituitary

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6
Q

GH deficiency in children

A

Short stature

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7
Q

GH deficiency in adults

A

Reduced muscle mass and performance

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8
Q

LH deficiency in men

A

Hypogonadism, reduced sperm count

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9
Q

LH deficiency in women

A

Hypogonadism, amenorrhoea

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10
Q

FSH deficiency

A

Infertile

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11
Q

TSH deficiency

A

Hypothyroidism

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12
Q

ACTH deficiency

A

Loss of pigmentation

Hypoadrenalism

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13
Q

Prolactin deficiency

A

Rare

Sheehan’s Syndrome - failure of lactation

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14
Q

Effects of TSH

A

Synthesis of Thyroglobulin (Tg)
Iodide ion uptake from blood into thyroid cells
Iodination of tyrosine residues on Tg - producing T4 and T3

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15
Q

T4

A

Thyroxine

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16
Q

T3

A

3,5,3’-Triiodothyronine

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17
Q

Predominantly circulating thyroid hormone

A

T4

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18
Q

Biologically active thyroid hormone

A

T3

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19
Q

Target for ACTH

A

Adrenal Gland
Adipocytes
Melanocytes

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20
Q

Target for GH

A

All tissues

Particularly liver

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21
Q

Target for FSH and LH

A

Gonads

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22
Q

Target for TSH

A

Thyroid gland

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23
Q

Zona glomerulosa

A

Release of Aldosterone

Outermost layer of adrenal cortex

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24
Q

Zona fasciculata

A

Release of cortisol

Middle layer of adrenal cortex

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25
Q

Zona reticularis

A

Release of DHEA

Innermost layer of adrenal cortex

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26
Q

Sella Turcica

A

Bone within which the hypothalamus sits

“Turkish cellar”

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27
Q

Symptoms of upward extending enlarged pituitary

A

Headache
Loss of visual acuity
Bitemporal hemianopia
(Compression of optic chiasm)

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28
Q

Enlarged pituitary causes

A

Headache

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29
Q

Causes of Hypothyroidism

A

Autoimmune - Hashimoto Thyroiditis
Ablative therapy (destruction of thyroid tissue)
Iodine deficiency
Idiopathic

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30
Q

Symptoms of Hypothyroidism

A 
Fatigue
Weight gain
Cold intolerance
Constipation
Menstrual irregularity
Joint pain and muscle cramps
Infertility
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31
Q

Signs of Hypothyroidism

A 
Hypothermia 
Periorbital puffiness
Oedema 
Hypothermia 
Rough, dry skin
Bradycardia
Peripheral neuropathy (delayed relaxation of ankle jerk)
Loss of outer 1/3 of eyebrow
Hoarseness
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32
Q

Function of thyroid hormones

A

Increase BMR
Long bone growth and Neural maturation
Increase sensitivity of body to catecholamines

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33
Q

Myxoedema Coma

A

End stage hypothyroidism (if poorly controlled)
Elderly, obese female becoming increasingly withdrawn /sleepy/confused.
Slips into a coma

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34
Q

Lab results for primary hypothyroidism

A

Low T4
High TSH
Hyponatraemia
Raised LFTs (Bilirubin, lactate dehydrogenase, creatinine kinase, ALT)

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35
Q

Euthyroid Sick Syndrome

A

Low T3
Normal T4
Normal or low TSH

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36
Q

Cause of hyperthyroidism with low TSH

A 
Graves Disease (Autoimmune, thyroid stimulating antibodies)
Nodular Goitre (older people)
Hyperemesis gravidarum
Post partum thyroiditis
Post viral thyroiditis
Drugs (amiodarone)
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37
Q

Cause of hyperthyroidism with high TSH

A

Resistance to thyroid hormone
Drugs (amiodarone, heparin)
TSH secreting pituitary adenoma
Neonatal period

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38
Q

Signs/Symptoms of Hyperthyroidism

A 
Heat intolerance and sweating 
Bulging eyes 
irregular Periods
Fatigue
Weight loss (increased appetite)
Increased bowel movements
Palpitations
Tremor 
Poor concentration
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39
Q

Treatment of mild hyperthyroidism

A

Propanolol

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40
Q

Why is Propanolol used in treatment of mild hyperthyroidism?

A

Blocks action of catecholamines (which is increased by XS cortisol)
Non-specific, acts on all cells in the body

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41
Q

Treatment of Graves disease

A

Antithyroid medications
(Radioactive Iodine - isolation, not good for families)
Thyroidectomy

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42
Q

Treatment of nodular goiters/adenomas causing hyperthyroidism

A

Radioiodine therapy

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43
Q

Why does Addison’s Disease cause hyperpigmentation?

A

High ACTH
Gives rise to MSH
Stimulates melanocytes

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44
Q

Why does Addison’s Disease cause anorexia?

A

High ACTH
Gives rise to MSH
Inhibits appetite

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45
Q

Signs/Symptoms of Addison’s disease

A 
Hyperpigmentation
Anorexia/Weight loss
Hyperkalaemia 
Hyponatraemia 
Weakness and fatigue 
Sexual dysfunction
Hypotension
Dehydration
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46
Q

Causes of Addison’s Disease

A 
Granulomas in adrenals (sarcoidosis, TB, fungal infection)
Shrunken adrenals (Autoimmune Adrenalitis, IDDM, 
Metastatic cancer 
Secondary to pituitary problem

Plus Amyloidosis and Haemochromatosis

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47
Q

Lab findings in Addison’s Disease

A 
Hyperkalaemia
Hyponatraemia 
Low cortisol
High ACTH = primary
Low ACTH = secondary
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48
Q

Synacthen Test

A

Measure serum cortisol
Administer Synacthen and wait 60 minutes
Measure serum cortisol

Normally, serum cortisol should double in 60 minutes

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49
Q

Treatment of Addison’s Disease

A

Cortisol replacement - Hydrocortisone

Aldosterone replacement - Fludrocortisone

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50
Q

Causes of Cushing’s Disease

A

Pituitary tumour (secreting ACTH)
Drugs - exogenous corticoids
Adrenal adenoma/carcinoma (secreting Cortisol)

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51
Q

What is Cushing’s Syndrome?

A

Hypercortisolism

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52
Q

Symptoms of Cushing’s Syndrome specific to men

A

Erectile dysfunction

Decreased libido and fertility

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53
Q

Signs/Symptoms of Cushing’s Syndrome

A 
Weight gain/Obesity 
Fatty deposits (moon face and hump back)
Thin skin (bruises easily)
Increased thirst and urination
Fatigue
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54
Q

Complications of Cushing’s Syndrome

A 
Increased risk of infection
T2DM
Bone loss/fracture
Kidney stones
Enlargement of pituitary tumour 
Hypertension (A and NA cause vasoconstriction)
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55
Q

What is pheochromocytoma?

A

Rare tumour of adrenal gland tissue

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56
Q

5Ps of Pheochromocytoma

A 
Pressure (Hypertension) - 90%
Pain - 80%
Perspiration - 71%
Palpitation - 64%
Pallor - 42%
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57
Q

Classic Triad of Pheochromocytoma

A

Palpitations
Perspiration
Pain

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58
Q

Absorptive state occurs

A

0-4 hours after a meal

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59
Q

Processes which occur during absorptive state:

A

TAG synthesis
Glycogenesis
Glycerol synthesis
Protein synthesis

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60
Q

How does pancreatic glucokinase differ from other hexokinases?

A

Not inhibited by its product - Glc-6-P

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61
Q

GLUT2

A

Glc transporter found in liver and pancreas
Low affinity
Works at high [Glc]

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62
Q

Glucokinase

A

Glc –> Glc-6-P

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63
Q

Where is UDP-glucose phosphorylase located?

A

Liver

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64
Q

UDP-Glucose Phosphorylase

A

Glc-6-P –> UDP Glc

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65
Q

PP-1 is activated by:

A

Insulin

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66
Q

Effect of PP-1

A

Upregulates glycogen production

Downregulates glycogenolysis

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67
Q

GLUT4

A

High affinity glucose transporter
Found in adipose tissue and muscle
Works at low [Glc]

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68
Q

Lipoprotein lipase

A

Cuts fatty acids from TAGs and transports them across capillary wall into cells

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69
Q

Lipoprotein Lipase is found in which cells

A

Luminal surface of capillary cells

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70
Q

Function of brown fat

A

Thermoregulation,

Protection against metabolic disease

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71
Q

Effect of exercise on GLUT4

A

Increase in number

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72
Q

GLUT4 is activated by:

A

Insulin

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73
Q

Function of carnitine shuttle

A

Allows Acetyl CoA to cross mitochondrial membrane so that it can enter the TCA cycle

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74
Q

Anabolism

A

Construction - consumes energy

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75
Q

Catabolism

A

Destruction - releases energy

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76
Q

Amino acids and glucose delivered to liver via

A

Hepatic Portal Vein

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77
Q

How do dietary TAGs reach the bloodstream?

A

Packaged into chylomicrons
Enter lacteals
Pass through thoracic duct into bloodstream

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78
Q

Action of insulin during Absorptive State

A

Uptake of amino acids and glucose into tissues
Uptake of TAGs into adipose tissues
Conversion of glucose to glycogen (activates glycogen synthase)

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79
Q

Action of glucocorticoids in post-absorptive state

A

Breakdown of protein and TAGs into glucose

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80
Q

Action of epinephrine in post-absorptive state

A

Breakdown of protein, glycogen and TAGs into glucose

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81
Q

Action of glucagon in post-absorptive state

A

Breakdown of glycogen into glucose

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82
Q

When does the body enter post-absorptive state?

A

After absorptive state

When enterocytes stop supplying portal hepatic circulation with glucose.

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83
Q

pK of a buffer

A

pH at which the buffer works best to resist changes in either direction.

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84
Q

Buffers found in renal tubules

A

Phosphate

Ammonia

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85
Q

3 Mechanisms of Renal Compensation

A

Bicarbonate reabsorption
Net Acid Secretion
Buffers (Phosphate and Ammonia)

86
Q

Causes of respiratory acidosis

A

Asthma, COPD

87
Q

Renal response to long term acidosis

A

Reabsorption of bicarbonate
Secretion of H+
Synthesis of ammonia

88
Q

Cause of Metabolic Acidosis

A

Diabetic Ketoacidosis

89
Q

Immediate compensation for acidosis

A

Buffering in bloodstream

90
Q

Time for respiratory response to occur in acidosis/alkalosis

91
Q

Time for renal response to occur in acidosis/alkalosis

92
Q

Kussmaul respiration

A

Deep breathing pattern which drives CO2 below normal levels

93
Q

Respiratory response to metabolic acidosis

A

Low pH detected by chemoreceptors in brainstem

Initiates deep breathing pattern (Kussmaul) to drive CO2 below normal level

94
Q

Chemoreceptors which detect pH change in the blood are located…

A

Ventrolateral surface of the medulla

95
Q

Factors which increase H+ secretion by kidneys

A 
Increased HCO3- filtration by glomerulus
Decreased extracellular volume (dehydration)
Low blood pH
High blood CO2
Low K+
Aldosterone
96
Q

Cells in the renal tubules responsible for H+ secretion and HCO3- reabsorption

A

Alpha intercalated cells

97
Q

Cells in renal tubules responsible for Na+ reabsorption and K+ secretion

A

Principal Cells

98
Q

Effects of aldosterone

A

Increased K+ and H+ in urine

Increased HCO3- and Na+ in blood

99
Q

Transporters activated by aldosterone

A

Na+/H+ ATPase exchange (in apical surface - lining lumen of tubule)
Na+/K+ ATPase exchange (on capillary membrane)

100
Q

Normal anion gap

A

HCO3- loss

101
Q

Anion Gap

A

(Na+) - ((Cl-)+(HCO3-))

Used to determine presence of unmeasured ions

102
Q

Increased anion gap

A

Accumulation of organic acid (H+ and A-) or impaired H+ secretion

103
Q

Mechanisms for normal anion gap

A

Inorganic addition - ingestion/infusion of inorganic acid (e.g. HCl)

GI Base loss - severe diarrhoea, small bowel fistula, surgical diversion of urine into bowel

Renal base loss AND acid secretion

104
Q

Mechanisms for increased anion gap

A 
Increased ketones (DKA or starvation ketosis)
Lactic acidosis 
Renal failure (increased organic acids due to lack of buffering)
Exogenous acid load (salicylate, methanol, ethylene glycol poisoning)
105
Q

Effect of surgical diversion of urine into gut (bladder cancer) on bowel mucosa

A

Mucosa secretes KHCO3 to buffer H+ from urine

106
Q

Anions raised in DKA

A

Acetoacetate and beta-OH butyrate

107
Q

Anions raised in starvation ketosis

A

Acetoacetate and beta-OH butyrate

108
Q

Anions raised in lactic acidosis

109
Q

Anions raised in renal failure

A

Organic acids

110
Q

Methanol poisoning is commonly seen in…

A

Alcoholics

111
Q

Ethylene glycol poisoning is commonly seen in..

A

Alcoholics

112
Q

Anion raised in salicylate poisoning

A

Salicylate

113
Q

Anion raised in methanol poisoning

114
Q

Anions raised in Ethylene glycol poisoning

A

Glycolate and oxalate

115
Q

Symptom of methanol poisoning

A

Visual disturbance

116
Q

Sign of ethylene glycol poisoning

A

Oxallate Crystalluria

117
Q

Ketones in ketoacidosis produced by…

A

Deamination of amino acids AND

Breakdown of fatty acids

118
Q

Blood ketones in DKA

119
Q

Blood glucose in DKA

A

> 11mmol/L

120
Q

Leukocytes in DKA?

A

Increased (stress response)

121
Q

Ketones on urine dipstick in DKA

122
Q

K+ depletion in DKA does not cause hypokalaemia because…

A

Patient is usually dehydrated

123
Q

Treatment of DKA

A

0.9% saline (replace lost fluids)
Insulin (0.1U/Kg/Hr)
Replace and monitor electrolytes
Restore acid:base balance

124
Q

Considerations for Insulin treatment in DKA

A

SLOW infusion - since hypokalaemia may cause cerebral oedema

Monitoring of K+ - since insulin increases cell permeability to K+, K+ enters cells causing hypokalaemia

125
Q

Cause of PROXIMAL renal tubular acidosis

A

Defect in HCO3- reabsorption

126
Q

Causes of DISTAL renal tubular acidosis

A

“Classical” - Defect in H+-ATPase pump

“Hyperkalaemia” - Defect in Na+ transport across apical membrane, too little Na+ in cell for exchange for K+ in blood

127
Q

Causes of respiratory alkalosis

A 
Prolonged hyperventilation:
Anxiety
Drugs which stimulate respiratory centre (caffeine, nicotine)
Brain disorders 
Chronic liver disease
128
Q

Electrolyte imbalance caused by hypovolaemic metabolic alkalosis

A

Hypokalaemia (low K+)

129
Q

Why does hypokalaemia cause H+ secretion?

A

Low K+ in blood
Little Na+/K+ exchange occurs across capillary membrane
Low K+ in intercalated cell
High K+/H+ exchange across apical membrane (K+ in, H+ out)
Increased H+ in tubular lumen for excretion

130
Q

Why is respiratory response to metabolic alkalosis limited?

A

Hypoventilation cannot be sustained due to hypoxia

131
Q

Renal response to hypovolaemic metabolic alkalosis

A

Na+ and HCO3- reabsorption in PCT
Aldosterone release
H+ secretion in DCT
NH3 synthesis

132
Q

Management of hypovolaemic metabolic alkalosis

A

Volume management - switch of volume conserving mechanisms which exacerbate alkalosis
K+ replacement

133
Q

Causes of normovolaemic metabolic alkalosis

A 
Conn's syndrome (hyperaldosteronism)
Cushing's syndrome (hypercortisolaemia - cortisol has similar effects to aldosterone)
Renal hypoperfusion (low GFR = low HCO3- filtration)

i.e. Anything which causes HCO3- retentio

134
Q

Symptoms of T1DM

A

Tiredness
Polydipsia
Polyuria
Weight loss

Candidal infection/Thrush (oral/genital due to high sugar environment)

135
Q

Criteria for DM diagnosis

A

HbA1c >6.5%
Fasting plasma glucose >7.0mmol/L
Random plasma glucose >11.0mmol/L

136
Q

GTT

A

Glucose tolerance test - Plasma glucose 2 hrs after administering 75g of glucose

137
Q

Symptoms of T2DM

A 
Polydipsia
Polyuria
Weight gain
Blurred vision
Candidal infection
138
Q

Incidence

A

Occurrence of new cases

139
Q

Prevalence

A

Proportion of cases in the population at a given time

140
Q

Ethnic group affected by Type 1 diabetes

A

Caucasian especially scandinavian

141
Q

Ethnic group affected by Type 2 diabetes

A

Non caucasians especially indigenous people, S. Indians and W. Indians

142
Q

Incidence of T1DM

143
Q

Incidence of T2DM

A

2/1000 per year

144
Q

Anti-Islet Cell Antibodies associated with T1DM

A

Anti-GAD65 (85%)
Anti-IA2 (55%)
Anti-Insulin (50%)
Anti-ZnT8 (50%)

145
Q

Immune Cells responsible for destruction of Beta Cells in T1DM

146
Q

Genes commonly associated with T1DM

A

HLA DR3/4 (Code for MHCs)

147
Q

Environmental factors affecting T1DM

A

Breastfeeding
Childhood infection
Neonatal colonisation

148
Q

Glucose level with increased risk of hyperosmolar coma

A

> 30mmol/L

149
Q

Hypoglycaemia

A

<4mmol/L (LOC occurs <2.5mmol/L)

150
Q

Normal BG

151
Q

Hyperglycaemia

152
Q

Blood pressure in DKA

153
Q

Oxygen saturation in DKA

A

Low (<92%)

154
Q

Glasgow Coma Scale in DKA

155
Q

Causes of death in DKA

A 
Cerebral oedema (due to hypokalaemia)
Other underlying conditions - sepsis, MI, acute respiratory syndrome
156
Q

Sulphonylureas

A

e.g. Gliclazide, Glibenclamide

Increased insulin release from beta cells in pancreas

157
Q

Cause of hypoglycaemia in non-insulin-dependent diabetes?

A

Sulphonylureas

Metformin

158
Q

Treatment of conscious (able to swallow) patient with hypoglycaemia

A

15-20g of quick acting CHO - repeat 3 times or until BG>4mmol/L
e.g. Dextrose, lucozade, sugar

When BG>4mmol/L, administer long acting CHO
e.g. biscuits, bread, milk

159
Q

Treatment of unconscious/aggressive patient with hypoglycaemia

A 
Parenteral glucose (20%: 75-100ml in 15 mins OR 10%: 150-200ml in 15 mins)
I/M Glucagon - 1mg

Check BG and repeat insulin infusion if BG<4mmol/L
Do not repeat glucagon

Follow up with long acting carbohydrate (or 10% glc if NBM)

160
Q

Formation of exudates in diabetic retinopathy

A

Hyperglycaemia causes osmotic damage to retinal pericytes.
Increased permeability of capillary walls
Leakage of proteins and lipids into retinal tissue
(+Foamy macrophages filled with lipid are deposited in under perfused capillary beds)

161
Q

Formation of microaneurysms in diabetic retinopathy

A

Hyerglycaemia causes osmotic damage to retinal pericytes

Weakening of capillary walls allows focal dilatation i.e. microaneurysm.

162
Q

Formation of cotton wool spots in diabetic retinopathy

A

Exudates and microaneurysms cause occlusion of vessels.

Ischaemic tissue appears white and fluffy i.e. cotton wool spot

163
Q

Vitreous haemorrhage in diabetic retinopathy

A

Ischaemic cells produce VEGF which stimulates formation of new vessels.
New vessels are thin walled and prone to bleeding.

164
Q

Complication of vitreous haemorrhage

A

Site-threatening

165
Q

Macular Oedema in diabetic retinopathy

A

Hyperglycaemia causes osmotic damage to retinal pericytes.
Weaker, more permeable capillary walls.
Leakage of fluid from capillary into retinal tissue

166
Q

Visual impairment in Macular Oedema

A

Loss of central vision

167
Q

Retinal Detachment in Diabetic Retinopathy

A

Collagen formation along the length of new, thin-walled vessels.
Form fibrotic bands which will contract to detach the retina

168
Q

Prevention of Vitreous Haemorrhage

A

Pan retinal photocoagulation

Anti-VEGF treatment

169
Q

Mesangial expansion

A

Endothelial expansion and inflammation caused by free radicals and cytokines

170
Q

Mechanism for Proteinuria in diabetic nephropathy

A

Trauma and damage to kidney nephrons due to increased GFR
Release of cytokines and free radicals
Causes mesangial expansion
Larger fenestrations, larger molecules inc. proteins filtered out of blood into kidney tubules

171
Q

Mechanism for Renal Failure in diabetic nephropathy

A

Hyperglycaemia activates RAAS
Vasoconstriction of efferent arteriole
Reduced perfusion of renal tubules - ischaemia
Atrophy of vessels which support renal function

172
Q

Mechanism for neuropathy in diabetes

A

Hyperglycaemia causes formation of sorbitol and fructose in Schwann cells
Loss of structure and function of schwann cells
Segmental demyelination

173
Q

Diabetic Amyotrophy

A

Painful wasting of quadriceps

Reflexes may be reduced or absent

174
Q

Acute, painful neuropathy

A

Burning or crawling pain in feet, shins or anterior thighs

May be worse at night

175
Q

Symmetrical mainly sensory, polyneuropathy

A

Loss of vibration sense and proprioception
Loss of temperature and pain sensation in extremities
May have unrecognised trauma (ulcers on feet)

176
Q

Multiple mononeuropathy

A

Isolated nerve palsies - often CNIII and CNVI

177
Q

Autonomic effects of neuropathy

A

GI - gastroparesis, diarrhoea, incontinence

Cardiovascular(vagus nerve affected) - postural hypotension, diminished vagal reflex, arrhythmia

Bladder - incomplete emptying and stasis

Male erectile dysfunction

178
Q

Purpose of measuring HbA1c

A

Assesses long term control of blood glucose (average over 6 weeks)
Useful in assessing risk of complications

179
Q

Short-acting insulin

A

Lispro, Aspart, Glulisine

180
Q

Long-acting insulin

A

NPH, Determir, Glargine

181
Q

Function of sclera

A

Attachment for extraocular muscles which move the eye

182
Q

Function of cornea

A

Refracts light entering the eye

183
Q

Function of choroid

A

Vascular layer

Nourishes outer layers of retina

184
Q

Structure of retina

A

Inner neural layer - containing photoreceptors

Outer pigmented layer - attached to choroid, continuing around whole inner surface of eye.

185
Q

Macula

A

Centre of retina

High acuity vision - for reading and driving

186
Q

Fovea

A

Depression in the centre of macula

Contains a high concentration of cones (light detecting cells) for sharp central vision

187
Q

What is Glaucoma?

A

Obstruction of drainage of aqueous humor.

Drainage normally occurs via trabecular mesh network.

188
Q

Blood supply of eye

A

Ophthalmic artery

Central artery of retina (supplies internal surface of retina - occlusion quickly causes blindness)

189
Q

Sign of glaucoma

A

Increase in size of optic disc

190
Q

Symptoms of retinal detachment

A

Blurred vision
Dark areas
Black or white flecks/strings in front of eyes

191
Q

Risk factors for retinal detachment

A

Family history
>40 years old
Trauma

192
Q

Features of background diabetic retinopathy

A

Dot and blot haemorrhages

Hard exudates

193
Q

Features of preproliferative diabetic retinopathy

A 
Venous beading 
Cotton wool spots 
Some new vessels 
More dot and blot haemorrhages 
Microaneurysms
194
Q

Features of proliferative diabetic retinopathy

A

More new vessels

195
Q

When do we refer diabetic retinopathy to secondary care?

A

Haemorrhages/Microaneurysms in 4 quadrants
Venous beading in 2 or more quadrants
IRMA (new vessels) in 1 or more quadrants

196
Q

When do we treat diabetic retinopathy?

A

Thickening of retina or hard exudates within 500micrometers of centre of macula
Zones of retinal thickening the size of the optic disc

197
Q

Ranibizumab

A

Monoclonal antibody which inhibits VEGF.

Used in treatment of diabetic retinopathy.

198
Q

Indication for hydrocortisone

A

Addison’s Disease (chronically low cortisol)

199
Q

ADRs for hydrocortisone

A

Weight gain
Fluid retention
Hyperglycaemia
Cushing’s (long term)

200
Q

Contraindications for Hydrocortisone

A

Immunosuppression
Diabetes
Active fungal infections

201
Q

Actions of Hydrocortisone

A

Upregulates gluconeogenesis - increases blood sugar

Suppresses inflammatory immune responses

202
Q

Binding site of Levothyroxine

A

Nuclear thyronine receptors

203
Q

What is levothyroxine?

A

Synthetic T4 which will be converted to T3 in the body

204
Q

Indication for levothyroxine

A

Hypothyroidism

205
Q

ADRs of levothyroxine

A 
Tremor 
Cardiac arrhythmias 
Excitability 
Diarrhoea 
Flushing
206
Q

Contraindications of Levothyroxine

A

Graves (Hyperthyroidism)
Ischaemic Heart disease
Thyrotoxicosis

207
Q

Indication for carbimazole

A

Hyperthyroidism

208
Q

MOA of Carbimazole

A

Thyroid peroxidase inhibitor

Enzyme which normally allows iodinisation of Tg, synthesising thyroid hormones

209
Q

ADRs of Carbimazole

A 
Fever
Headache
Rash
Joint pain
Taste disturbance
210
Q

Contraindication of Carbimazole

A

Warfarinised - drug may enhance anticoagulation

Year 2 (17 decks)

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