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Phase 2a Revision > Endocrinology > Flashcards

Endocrinology Flashcards

Diabetes Type 1 & 2 , DKA, HHS, Hypo/ Hyperglycaemia, Hypo/ Hyperthyroidism, Graves, Thyroid cancer, Hashimoto's, Cushing's syndrome /disease, Acromegaly, Prolactinoma, Conn's Syndrome, Addisons 1° &2° ,SIADH, Hypo/ Hyperkalaemia, Diabetes Insipidus, Hypo/ Hyperparathyroidism, Pheochromocytoma, Diabetes meds, Thyroid drugs, Steroids, Pituitary gland drugs

1
Q

What is Type 1 Diabetes?

A

This is insulin deficiency due to an autoimmune destruction of pancreatic B-cells

– The disease usually manifests in adolescence, sometimes after a viral infection.

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2
Q

Symptoms of Type 1 Diabetes?

A

– Hyperglycemia – low insulin leads to decreased glucose uptake by fat and muscle

– Weight loss, low muscle mass – unopposed glucagon leads to lipolysis and glycogenolysis

– Polyuria, polydipsia and glycosuria

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3
Q

Treatment of Type 1 Diabetes?

A

1) Insulin therapy – twice-daily insulin detemir is a common regime, but depends on patient’s diet and compliance
2) Monitor HbA1c every 3-6months

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4
Q

Diagnosis for Type 1 Diabetes?

A

The diagnosis of diabetes mellitus can be made using plasma glucose or a HbA1c sample[1].

– Plasma glucose or HbA1c must show evidence of diabetes of two separate occasions if asymptomatic:

Fasting glucose > 7.0 mmol/L
Random glucose/OGTT > 11.1mmol/L
HbA1c > 48mmol/mol (6.5%)

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5
Q

Acute Complication for Type 1 Diabetes?

A

Diabetic Ketoacidosis

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6
Q

What is Type 2 Diabetes and causes

A

This is non- insulin dependent/ resistant

– Arises in middle aged, obese adults due to decreased number insulin receptors due to failed secretion from pancreatic B- cells

– Progresses from impaired glucose tolerance

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7
Q

Risk of Type 2 Diabetes?

A

Obesity, lack of excercise + alcohol excess

– Stronger genetic influence than type 1 – high in Asians, men and the elderly

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8
Q

Diagnosis for Type 2 Diabetes?

A

The diagnosis of diabetes mellitus can be made using plasma glucose or a HbA1c sample[1].

Fasting glucose > 7.0 mmol/L
Random glucose/OGTT > 11.1mmol/L
HbA1c > 48mmol/mol (6.5%)

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9
Q

Treatment for Type 2 Diabetes

A

1) If HbA1c rises to 48mM

– Lifestyle modifications – diet, weight control + exercise

2) If HbA1c stays above 48mM

– Commence Metformin – aim for HbA1c < 48mM

3) If HbA1c rises >58mM …Dual, Triple therapy

– Add sulphonylurea or Pioglitazone or DPP -4 inhibitor or SGLT-2 inhibitor or insulin

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10
Q

Acute Complication for Type 2 Diabetes?

A

HHS

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11
Q

What is DKA?

A

This is an emergency which is characterized by severe hyperglycaemia and severe acidosis, due to lack of insulin.

– Due to the body being in starvation like state and excessive ketone body production.

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12
Q

Symptoms of DKA?

A

– Triad of drowsiness + dehydration + Unexplained vomiting
– Ketotic/ fruity breath, coma
– Deep breathing (Kussmaul hyperventilation)
- Tachycardia
- Weight loss
- Potassium imbalance

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13
Q

Diagnosis for DKA?

A

– Acidaemia (Venous pH <7.3 or HCO3– >15mM)
– Hyperglycaemia (glucose >11mM) or known diabetic
– Ketones >3mmol/L on a urine dipstick
- Serum U + E = Increase urea, creatinine, Decrease total and serum K+

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14
Q

Management for DKA?

A

Use the ABC approach
F = Fluids - IV Fluid resuscitation with saline

I = Insulin - Insulin infusion

G = Glucose - Dextrose infusion if < 14 mmol / L

P = Potassium - monitor serum k+

I = Infection - Treat underlying cause

c = Chart - fluid balance

k = ketones - monitor blood ketones/ bicarb.

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15
Q

Complications for DKA?

A

– Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia

– Cerebral oedema –> seen more in children/young adults, occurs 4-12 hours usually after treatment

–> Gives headache, confusion, visual disturbances due to raised ICP

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16
Q

Chronic complication for DM?

A

Microvascular = Retinopathy, Nephropathy, Erectile dysfunction, Neuropathy

Macrovascular = Atherosclerosis, Stable angina, ACS, stroke

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17
Q

What is HHS?

A
  • Marked hyperglycaemia
  • Hyperosmolality
  • No ketosis
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18
Q

HHS Pathophysiology?

A
  • Low insulin -> Increased gluconeogenesis -> hyperglycaemia but not enough to inhibit ketoneogenesis.
    • Hyperglycaemia -> Osmotic diuresis -> Dehydration
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19
Q

DKA pathophysiology?

A
  • Peripheral lipolysis -> Increase in free fatty acids -> oxidised to Acetyl CoA -> Ketone bodies = Acidosis
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20
Q

HHS Symptoms?

A

Diabetes +…

  • Confusion
  • Lethargy
  • Deydration
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21
Q

Hyperglycaemia pathophysiology?

A
  • Absence of insulin -> more catabolism -> more gluconeogenesis & decreased peripheral glucose uptake -> Hyperglycaemia
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22
Q

HHS diagnosis?

A
  • Random plasma glucose = >11mmol/L
  • Urine dipstick = glycosuria
  • U+E = Decrease total K+, Increase serum K+
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23
Q

HHS treatment?

A
  • Replace fluid
  • Insulin
  • Restore electrolytes e.g. K+
  • Low molecular weight heparin
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24
Q

Hyperthyroidism

A

increased levels of circulating thyroid hormone.
– It leads to increase in basal metabolic rate (due to increased synthesis of Na/K-ATPase)
– Increased sympathetic nervous system activity (due to increased B1-adrenergic receptors)

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25
Q

Hyperthyroidism symptoms?

A

– Weight loss despite increase appetite

– Heat intolerance and sweating

– Tachycardia + palpitations

– Tremor/anxiety

– Decreased muscle mass with weakness

– Bone resorption with hypercalcemia

– Hyperglycaemia

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26
Q

Hyperthyroidism signs

A 
– Fast pulse/atrial fibrillation
– Warm moist skin
– Thin hair
- Goitre
- Menorrhagia
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27
Q

Hyperthyroidism diagnosis

A

– TFT shows high T4, low TSH. High glucose and hypocholesterolaemia

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28
Q

Hyperthyroidism treatment

A

i) Beta-blockers – Propranolol gives control of symptoms due to high sympathetic activity

Propranolol + Carbimazole + Iodine

2nd line - Propylthiouracil

iii) Radioiodine
iv) Thyroidectomy – risk of recurrent laryngeal nerve injury + people become hypothyroid after

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29
Q

Graves disease

A

This is an autoimmune condition which is the most common cause of hyperthyroidism

– Autoimmune IgG antibody stimulates the TSH receptor antibodies increasing thyroid release

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30
Q

Graves disease symptoms

A

– Diffuse goitre as constant TSH stimulate leads to thyroid hyperplasia

– Pretibial myxoedema – shin fibroblasts express TSH receptor causing inflammation

– Exophthalmos (bulging of eyes) – fibroblasts behind orbit express the TSH receptor

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31
Q

Hashimoto thyroiditis

A

most common cause in regions where iodine levels are adequate
– Due to autoimmune destruction of thyroid gland by anti- TPO & Antithyroglobulin antibodies
- associated with Type I diabetes, Addison’s
- High TSH, Low T4

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32
Q

Hypothyroidism

A
  • marked by a lack of thyroid hormone

- based on decreased BMR and decreased sympathetic activity

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33
Q

Hypothyroidism symptoms

A 
– Increased weight with normal appetite
– Cold intolerance with no sweating
– Bradycardia
– Decreased mood
– Constipation
– lethargic
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34
Q

Hypothyroidism signs

A

– Slow reflexes and ataxia
– Cold dry hands
– Ascites/oedema
– Hypercholesterolemia

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35
Q

Hypothyroidism diagnosis

A
  • Primary = High TSH, Low T4

- Secondary = Low TSH, Low T4

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36
Q

Hypothyroidism treatment

A

Levothyroxine (T4)

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37
Q

Subclinical hypothyroidism

A

High TSH, Normal T4

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38
Q

De Quervian Thyroiditis

A

granulomatous thyroiditis after a viral infection

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39
Q

Thyroid Storm + Treatment

A

biggest complications of hyperthyroidism due to trauma

IV propranolol + Propylthiouracil + Dexamethasone (stops T4 –> T3) + Iodine solution

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40
Q

Cushing’s syndrome and disease

A

Syndrome = chronic cortisol excess
Disease = Caused by an ACTH secreting pituitary adenoma
More ACTH -> Adrenal cortex especially zona fasciculata stimulated -> More cortisol

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41
Q

Cushing’s syndrome causes

A

ACTH-independent causes: (gives low ACTH –> adrenal atrophy)
- steroids, adenoma

ACTH-dependent causes: (gives high ACTH –> adrenal hyperplasia)
- Cushing’s disease, Ectopic ACTH production from small cell lung cancer

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42
Q

Cushing’s syndrome symptoms

A

– Muscle weakness and breakdown
– Osteoporosis
– Immune suppression
– Hypertension

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43
Q

Cushing’s syndrome signs

A

– Abdominal striae- thinning of skin
– Poor wound healing
– Central obesity, buffalo hump
– Moon faced shape

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44
Q

Cushing’s syndrome diagnosis

A

– 1st line: Overnight dexamethasone test (48hr)
Normally cortisol is suppressed
low Dose Test - High cortisol = Cushing’s Syndrome
High Dose test - Low Cortisol = Cushing’s Disease
- High Cortisol - ACTH High= Ectopic ACTH
- ACTH low = Adrenal adenoma
-2nd line: 24-hour urinary free cortisol

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45
Q

Cushing’s syndrome Treatment

A

Stop steroids if iatrogenic, Transsphenoidal surgery, adrenalectomy

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46
Q

Pheochromocytoma

A

adrenaline producing tumour of the chromaffin cells

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47
Q

Pheochromocytoma symptoms

A

Triad of episodic headache, sweating and tachycardia (palpitations), with hypertension

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48
Q

Pheochromocytoma diagnosis

A

Increased plasma Metanephrine level
– Increased 24-hr Urine Catecholamines
– Abdominal CT/MRI scan to locate tumour

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49
Q

Pheochromocytoma treatment

A

– 1st line = alpha-blocker - phenoxybenzamine
- 2nd line = beta - blocker - Atenolol / Metoprolol
– Surgical excision to remove tumour

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50
Q

Conn’s syndrome

A

primary hyperaldosteronism due to an aldosterone producing adenoma

Secondary hyperaldosteronism = excess renin causing more Aldosterone - serum renin will be high

Big cause in 2° hypertension

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51
Q

Conn’s syndrome pathophysiology

A

excess production of aldosterone independent of the renin-angiotensin, causing increased sodium and water retention.
– It is characterized by high aldosterone and low renin (as high BP inhibits renin)

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52
Q

Conn’s syndrome symptoms

A
  • hypertension
  • hypokalaemia
  • Hypernatraemia
  • nocturia
  • polyuria
  • headache, anxiety
  • atrial fib.
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53
Q

Conn’s syndrome investigations

A

Aldosterone - Renin Ratio blood test -
High aldosterone , Low renin = 1°
High aldosterone , High renin = 2°
Plasma potassium - low

54
Q

Conn’s syndrome Treatment

A

– Conn’s syndrome –> laparoscopic surgery to remove adenoma

– Hyperplasia –> K+ sparing diuretics e.g. spironolactone

55
Q

Addison’s disease/ Primary insufficiency

A

(increased ACTH)
failure of adrenal gland to produce cortisol and aldosterone
- caused by TB, autoimmune disease

56
Q

Secondary adrenal insufficiency

A

(decreased ACTH)
caused by a factor extrinsic to the adrenal glands
– Most common cause is iatrogenic due to long term steroid therapy and adrenal suppression

57
Q

Addison’s disease symptoms

A

– Lack of cortisol –> hypotension, muscle weakness
– Lack of aldosterone –> dehydration, hypovolemia, hyponatremia, hyperkalaemia
– Metabolic acidosis
– Increased ACTH –> causes hyperpigmentation due to increase melanocyte stimulating hormone

58
Q

Addison’s disease Diagnosis

A 
1st line ACTH stimulation test 
(Short Synacthen test - No rise= Primary A.l)
( Long Synacthen test - No change
Primary =  High ACTH level
Secondary = low ACTH level
  • CT/ MRI of adrenals & Pituitary
59
Q

Addison’s disease Treatment

A

– Replace cortisol – hydrocortisone (glucocorticoid)

– Replace aldosterone – fludrocortisone (mineralocorticoid)

60
Q

Acromegaly

A

increased secretion of growth hormone from the anterior pituitary
– Most often due to a pituitary adenoma

61
Q

Acromegaly Symptoms

A
  • enlarged hands, tongue, jaw and feet
  • prominent forehead
  • profuse sweating
  • bitemporal hemianopia
62
Q

Acromegaly investigations

A

– 1st line is to check if Serum IGF-1 level is raised

  • Oral glucose tolerance test
  • MRI scan of pituitary fossa
63
Q

Acromegaly Treatment

A

– 1st line is transphenoidal surgery
– Octreotide – somatostatin analogue
– Pegvisomant – GH receptor antagonist
- Bromocriptine - Dopamine agonist

64
Q

Acromegaly complications

A
  • Secondary diabetes mellitus as GH induces gluconeogenesis

- Erectile dysfunction

65
Q

Prolactinoma

A

pituitary adenoma producing excess prolactin

66
Q

Prolactinoma causes

A
  • dopamine antagonists (reduce inhibition of prolactin)

- Primary hypothyroidism (TRH stimulates prolactin release)

67
Q

Prolactinoma symptoms

A

Women = Galactorrhoea, Amenorrhoea, Infertility
-> Raised prolactin inhibits GnRH which decreases LH, FSH, oestrogen and testosterone
Men = Erectile dysfuction, Less libido

68
Q

Prolactinoma Diagnosis

A
  • Prolactin levels

- MRI of pituitary gland

69
Q

Prolactinoma Treatment

A

– 1st choice is dopamine agonists to reduce prolactin secretion e.g. Bromocriptine/Cabergoline
- 2nd line = Transsphenoidal Resection Surgery of pit. gland

70
Q

SIADH

A

excessive ADH secretion - causing water to be reabsorbed in collecting duct

71
Q

SIADH Causes

A

ectopic ADH production (e.g. small cell lung carcinoma)

– CNS trauma + Drugs (Thiazide diuretics, SSRIs (Sertraline), NSAIDs)

72
Q

SIADH Symptoms

A

– Hyponatremia

  • Low osmolaIity
  • Muscle aches & cramps
  • neuronal swelling and cerebral oedema
  • Seizures & Headaches
73
Q

SIADH Diagnosis

A
  • Urine sodium = high
  • Urine osmolality = high
  • Euvolemic
  • Low Na+
74
Q

SIADH Treatment

A

– Water restriction

– ADH receptor antagonists [Tolvaptan]

75
Q

Diabetic Insipidus

A

Production of too much dilute urine due to poor water reabsorption from kidneys due to lack of ADH.
Split into Cranial and Nephrogenic

76
Q

Diabetic Insipidus Pathophysiology

A
  • > Large volumes of dilute urine due to reduced ADH
  • > Less Secretion from posterior pituitary [Cranial]
  • > Impaired response of kidneys to ADH [Nephrogenic]
77
Q

Cranial causes

A
  • Idiopathic
  • Neurosurgery
  • Tumour/ Trauma
  • Infection (Encephalitis)
78
Q

Nephrogenic causes of Dl

A
  • Inherited
  • Metabolic [Low K+, High Ca2+]
  • Drugs [Lithium]
79
Q

Diabetic Insipidus Symptoms

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Dilute urine
80
Q

Diabetic Insipidus Diagnosis

A

– Water deprivation test or Desmopressin Stimulation test - assess urine Osmolality

Cranial (Neurogenic) Dl = After Desmopressin - level is high, After fluid depriv. - level is low

Nephrogernic DI = After Desmopressin & Fluid deprive - level is low

81
Q

Diabetic Insipidus Treatment

A
  • Rehydration
    – Cranial DI –> Desmopressin - replace ADH
    – Nephrogenic DI –> Bendroflumethiazide – acts as an anti-diuretic
82
Q

Hyperkalaemia

A

> 5.5 mmol/L

83
Q

Hyperkalaemia Aetiology

A
  • > Impaired excretion: - AKI / - Drugs (NSAIDs, ACE-I, Beta- blockers) / - Addison’s
  • > Increased Intake: - IV K+ therapy / - Increased dietary intake
  • > Shift to extracellular: - Metabolic acidosis (Rhabdomyolysis) /
  • Decreased insulin
84
Q

Hyperkalaemia Symptoms

A
  • Fatigue
  • Light- headedness
  • Weakness
  • Chest pain
  • Palpitations
85
Q

Hyperkalaemia Signs

A
  • Ventricular Tachycardia
86
Q

Hyperkalaemia ECG

A
  • > No P waves
  • > Prolonged PR interval
  • > Wide QRS interval
  • > Tall tented T waves
87
Q

Hyperkalaemia Diagnosis

A
  • ECG

- Bloods -> FBC, U+E

88
Q

Hyperkalaemia Treatment

A
  • ABC
  • Cardiac monitoring
  • Calcium Gluconate
  • Insulin + Dextrose or Nebulised salbutamol
89
Q

Hypokalaemia

A

< 3.5 mmol/L

90
Q

Hypokalaemia Aetiology

A
  • > Increased Excretion: - Renal disease / - Drugs (Thiazide, Loop diuretics, Laxatives) / - GI Loss /
  • Conn’s syndrome
  • > Decreased Intake: - Dietary deficiency
  • > Shift to intracellular: - Metabolic alkalosis / - Drugs (B2 agonist = SABA & LABA)
91
Q

Hypokalaemia symptoms

A

Asymptomatic

92
Q

Hypokalaemia signs

A

Rhabdomyolysis

93
Q

Hypokalaemia ECG

A
  • > Prolonged PR interval
  • > ST depression
  • > Flat T wave inversion
  • > Prominent U waves
94
Q

Hypokalaemia Treatment

A
  • Potassium - IV
95
Q

Hyperparathyroidism

A

Primary Hyperparathyroidism - excess PTH due to a disorder of the parathyroid gland itself e,g. tumour

Secondary Hyperparathyroidism - excess PTH due to a disease extrinsic to gland - low vit D → less Ca2 + absorption → more PTH

Tertiary hyperparathyroidism - prolonged secondary hyperparathyroidism, causing glands to act autonomously

96
Q

Hyperparathyroidism Causes

A

Primary Hyperparathyroidism = parathyroid adenoma, parathyroid hyperplasia

Secondary Hyperparathyroidism = chronic kidney disease / Low Vit. D
– Renal failure → decreased phosphate excretion →Phosphate binds serum Ca2+
– Less free calcium stimulates parathyroid glands to secrete excess PTH

Tertiary hyperparathyroidism = – Leads to increased Calcium from high PTH secretion → leads to hyperplasia of gland
– Decreased Phopshate and Vitamin D

97
Q

Hyperparathyroidism Symptoms

A
  • > Bone pain
  • > Renal stone
  • > Physic Moans
  • > Abdominal Groans
  • > Hypercalcaemia
98
Q

Hyperparathyroidism Diagnosis

A 
- PTH/ blood test : High PTH...
Primary = + High Ca2+
Secondary = + Low Ca2+
Tertiary = + High Ca2+
LOW phosphates, Low Vit D
99
Q

Hyperparathyroidism Treatment

A

Primary = Surgical removal , Bisphosphonates

Secondary = Calcium correction

Tertiary = Cinacalcet

100
Q

Hypoparathyroidism

A

Primary = Gland failure

  • > Autoimmune
  • > Congenital (DiGeaorge syndrome)

Secondary = Pituitary gland dysfunction
-> Low Mg (required for PTH secretion)

Tertiary = Hypothalamic dysfunction

101
Q

Hypoparathyroidism Signs & Symptoms

A
  • > Chvostek’s sign = Facial nerve tap induces spasm
  • > Trousseau’s sign = BP cuff causes wrist flexion
  • Convulsions
  • Arrhythmias
  • Tetany
  • Spasms
  • Numbness
102
Q

Hypoparathyroidism Investigations

A

Bloods =

  • > Low PTH
  • > Low Ca2+
  • > High Phosphate
103
Q

Hypoparathyroidism Treatment

A
  • IV Calcium

- AdCal D3 - Calcitriol

104
Q

Type 1 Diabetes pathophysiology

A

– T lymphocytes attack B - cells in islets of langerhans, with autoantibodies against insulin present -> Hyperglycaemia

  • Continuous breakdown of glycogen from liver -> glycosuria

– It is associated with HLA-DR3 and HLA-DR4

105
Q

What are the normal glucose levels?

A

4.4 - 6.1 mmol/ L

106
Q

Where is insulin produced?

A

By Beta cells in the Islets of Langerhans in the pancreas

107
Q

Two ways insulin reduces the blood sugar?

A

1) causes cells to absorb glucose from blood and uses it as fuel
2) causes muscle and liver cells to absorb glucose from blood and stores it as glycogen

108
Q

Where is glucagon produced?

A

Produced by alpha cells in the Islets of langerhans in the pancreas

109
Q

What does glucagon do?

A

Tells liver to break down glycogen into glucose (glycogenolysis).
Also tells liver to convert Proteins and fats to glucose (gluconeogenesis).

110
Q

Ketogenesis?

A

Where there’s less glucose supply and glycogen stores (eg. fasting), liver converts fatty acids to ketones

111
Q

Macrovascular complications of Diabetes Type 1

A

CAD, Hypertension, Stroke

112
Q

Microvascular complications of T1 DM

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
113
Q

Type 2 DM Presentation

A
  • Fatigue
  • Polydipsia
  • Polyuria
  • Glycosuria
  • Weight loss
114
Q

Cause of hypothyroidism

A
  • Lithium

- Amiodarone drug

115
Q

Primary Hyper/ Hypo thyroidism pathology

A

Due to thyroid itself producing high / low thyroid hormone

116
Q

Secondary Hyper /Hypo thyroidism

A

Disorder with pituitary gland causing over/ under Stimulation of TSH causing high/ low thyroid hormone

117
Q

Where is adrenaline made?

A

by Chromaffin cells in the adrenal medulla

118
Q

Ca2 + levels in Hyperparathyroidism

A

1° = High

2° = low/ Normal

3° = High

119
Q

Renin - Angiotensin system

A
  • Juxtaglomerular cells in afferent arterioles of kidneys sense BP levels

In low BP = they secrete renin

Liver secretes Angiotensinogen

  • Renin converts Angiotensinogen → Angiotensin 1
  • Angiotensin 1 turns to Angiotensin 2 in the lungs with the help of Angiotensin converting enzymes (ACE)
  • Angiotensin 2 Stimulates release of aldosterone from Zona Glomerulusa in the adrenal glands
120
Q

Functions of cortisol?

A
  • Inhibits immune system
  • Inhibits bone formation
  • Raises blood glucose
  • Increases metabolism
  • increases alertness
121
Q

In Diabetes What is the
plasma glucose - Random & Fasting?

HbA1c?

Oral glucose tolerance test?

A

Plasma glucose:
Random: > 11 mmol/L
Fasting: >7 mmol/ L

HbA1c : >48 mmol/ L

Oral glucose test: give glucose drink, after 2 hrs plasma glucose: 11mmol/L

122
Q

Pre -diabetic diagnosis- What is the:

HbA1c range?

Impaired fasting glucose?

Impaired glucose tolerance?

A

HbA1c = 42-47 mmol /mol

Impaired fasting Glucose - Fasting glucose: 6.1-6.9 mmol/L

Impaired glucose tolerance- take oral glucose tolerance test
Plasma glucose after 2 hours = 7.8-11.1mmol/L

123
Q

BIGUANIDES

e.g. + What it does? + Side effects

A

e.g. Metformin

Prevents production of glucose in liver, increases insulin sensitivity.

S. E = Lactic acidosis , Gl disturbance

124
Q

SULFONYLUREAS

e.g. + What it does? + Side effects

A

e.g. Glipizide

Cause insulin secretion by binding to ATP - sensitive Potassium channels.

S. E = Hypoglycaemia , Weight gain

125
Q

THIAZOLIDINEDIONES (Glitazone)

e.g. + What it does? + Side Effects

A

e.g. Pioglitazone

Boosts insulin sensitivity.

S.E = Fluid retention, Weight gain, Worsening heart Failure

126
Q

SGLT 2 inhibitors (Sodium -glucose co-transporter-2)

e.g. + What it does? + Side Effects

A

e.g. Dapagliflozin

Prevents kidneys from reabsorbing glucose back into blood.

S. E = Risk of UTIs , Diabetic Ketoacidosis when used with insulin

127
Q

DPP 4 -inhibitors

e.g.+ What it does? + Side Effects

A

e.g. Sitagliptin

Blocks DPP4 enzymes → More incretin hormones → Stimulates insulin secretion.

S. E = Hypoglycaemia, Gl upset

128
Q

GLP1 Analogues

e.g. + What it does? + Side Effects

A

e.g. Exenatide

Incretin hormone mimics.

S. E = Hypoglycaemia , Gl upset , Increased risk of pancreatitis if used with DPP-4 inhibitors

129
Q

Hypercalcaemia

Causes

Diagnosis

Management

A

> 2.65 mmol/L

Causes = 1° & 3° Hyperpara., Vit.D&A, Osteolytic bone lesions

Ix = ECG (Shortened QT interval, J waves), Bone profile

Tx = IV Fluids, Bisphosphonates

130
Q

Thyroid Function Test Diagnosis results

A

Hyper / Graves = Low TSH, High T4 - TSH receptors antibodies

I° Hypo. (Hash.) = High TSH, Low T4 - (Anti- TPO antibodies)

2° Hypo. = Low TSH, Low T4

131
Q

Carbimazole

A

block thyroid Peroxidase

Adverse S. E = Agranulocytosis

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