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General study MD3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the physiological causes of early morning hyperglycemia in insulin-dependent individuals?

A

Physiological increase in growth hormone levels in the early morning hours stimulates gluconeogenesis and leads to a subsequent increase in insulin demand that cannot be met in insulin-dependent patients, resulting in elevated blood glucose levels.

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2
Q

Diagnostic criteria for diabetes mellitus

A

Random blood glucose level >= 200mg/dL in patients with symptoms of hyperglycemia (ie. polydipsia, polyuria, polyphagia, unexplained weight loss) or hyperglycemic crisis
OR
>= 2 abnormal test results for hyperglycemia in asymptomatic individuals

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3
Q

Describe the oral glucose tolerance test

A

Measurement of fasting plasma glucose and blood glucose 2 hours after the consumption of 75g of glucose

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4
Q

Describe Hemoglobin A1C test

A

HbA1C test measures the concentration of glycated hemogloblin A1 in red blood cells (glucose in the blood binds to hemoglobin). HbA1C test measures the average blood glucose levels of the prior 8-12 weeks

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5
Q

Which conditions and treatments may alter HbA1C results?

A

Sickle cell trait
CKD
Increased RBC lifespan (e.g. iron and/or vitamin B12 deficiency, splenectomy, aplastic anemia
Heavy alcohol use
Decreased RBC lifespan (e.g. due to acute blood loss, sickle cell trait, thalassemia, G6PD deficiency, cirrhosis, hemolytic anemia, splenomegaly, antiretrovial drugs)
Increased erythropoiesis (EPO therapy, pregnancy, iron supplementation)

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6
Q

How often should you check HbA1C in a diabetic patient?

A

At least every 3-6 months

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7
Q

Fasting glucose level target in diabetes

A

80-130 mg/DL (4.4-7.2 mmol/L)

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8
Q

Contraindications for metformin

A

Severely impaired renal function (eGFR <30mL/minute/1.73m2)
Acute or chronic metabolic acidosis (including ketoacidosis)
Hypersensitivity to metformin

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9
Q

Name glucose dependent and glucose independent insulinotropic agents

A

Glucose-dependent: GLP1 agonists, DPP4 inhibitors
Glucose-independent: Sufonylureas, meglitinides

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10
Q

How do insulinotropic agents work?

A

Stimulate the secretion of insulin from pancreatic B cells - either stimulated by elevated blood glucose levels (postprandially) or irrespective of blood glucose levels (risk of hypoglycemia)

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11
Q

Common contraindications of antidiabetic drugs

A

T1DM
Pregnancy and breastfeeding (all contraindicated - should be substituted with human insulin)
Renal failure (if GFR<30ml/min DPP4 inhibitors, incretin mimetic drugs, meglitinides and thiazolidinediones may be administered)
Major surgery under general anesthesia
Acute conditions requiring hospitalisation (infections, organ failure)
Elective procedures associated with an increased risk of hypoglycemia (periods of fasting)

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12
Q

How do biguanides (metformin) work?

A
  • Enhances effect of insulin
  • Decreases hepatic gluconeogenesis and intestinal glucose absorption
  • Increases peripheral insulin sensitivity which increases peripheral glucose uptake and glycolysis
  • Reduces LDL, increases HDL
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13
Q

Clinical characteristics of metformin:

A
  • Lowers HbA1C by 1.2-2% over 3 months
  • Weight loss
  • No risk of hypoglycemia
  • Reduces risk of macroangiopathic complications
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14
Q

Side effects of metformin

A
  • Metformin associated lactic acidosis
  • GI symtoms (N+V, diarrhoea, vomiting, adominal pain, flatulence
  • Severe symptoms: muscle cramps, hyperventilation, apathy, disorientation, coma
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15
Q

How do thiazolidinediones (glitazones) work?

A

Increased storage of fatty acids in adipocytes, decreased free fatty acids in circulation, increased glucoe utilisation and decreased hepatic glucose production

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16
Q

Side effects of glitazones

A

Increased risk of heart failure
Increased risk of fractures (osteoporosis)
Fluid retention and oedema
Weight gain
Rosiglitazone: Increased risk of CV complications like cardiac infarction or death

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17
Q

How do sulfonylureas work?

A

Block ATP-sensitive potassium channels of the pancreatic B cells -> depolarisation of the cell membrane -> calcium influx -> insulin secretion

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18
Q

Contraindications to sulfonylureas

A

Beta blockers (can mask hypoglycemic symptoms while lowering serum glucose levels)
Severe CV comorbidity
Obesity
Sulfonamide allergy
Liver and kidney failure

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19
Q

Names of sulfonylureas

A

Chlorpropamide
Tolbutamide
Glyburide
Glipizide
Glimepiride

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20
Q

How do glucagon-like peptide 1 receptor agonists (incretin mimetics) work?

A

Incretin mimetic drugs bind to the GLP-1 receptors and are resistant to degradation by DPP4 enzyme -> increased insulin secretion, decreased glucagon secretion, slow gastric emptying (increased feeling of satiety, decreased weight)

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21
Q

Side effects of GLP1 receptor agonists

A

N+V
Strong feeling of satiety
Pancreatitis and potentially pancreatic cancer

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22
Q

Contraindications for GLP1 receptor agonists

A

GI motility disorders
Chronic pancreatitis or a family history of pancreatic tumors
Personal or family history of MTC or multiple endocrine neoplasia syndrome type 2 (MEN 2)

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23
Q

How do Dipeptidyl peptidase-4 inhibitors (gliptins) work?

A

Indirectly increase the endogenous incretin effect by inhibiting the DPP-4 that breaks down GLP-1 -> increased insulin secretion -> decreased glucagon secretion, delayed gastric emptying

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24
Q

Side effects of DPP-4 inhibitors

A

GI symptoms
Arthralgia
Nasopharyngitis and URTI
Increased feelings of satiety
Urinary infections (mild)
Increased risk of pancreatitis
Worsening renal function, acute renal failure
Headaches, dizziness

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25
Q

How do SGLT2 inhibitors (glifozins) work?

A

Reversible inhibition of SGLT2 in the proximal tubule of the kidney -> decreased glucose reabsorption in the PCT of the kidney -> glycosuria and polyuria

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26
Q

Side effects of SGLT2 inhibitors

A

UTIs, genital infections (vulvovaginal candidiasis, balantitis) due to glucosuria
Dehydration, weight loss, orthostatic hypotension
Severe diabetic ketoacidosis

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27
Q

Describe a hyperosmolar hyperglycemic state

A

Condition primarily seen in T2DM due to extreme hyperglycemia. Unlike in DKA, there is some insulin available to suppress fat breakdown so ketosis does not result, rather, severe hyperglycemia (>600mg/dL) may develop

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28
Q

Clinical manifestations of hyperosmolar hyperglycemic state

A

Polyuria, polydipsia, nausea, vomiting, volume depletion and eventually mental status changes and coma

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29
Q

Describe diabetic ketoacidosis

A

Primarily seen in patients with T1DM
Caused by insufficient insulin levels (often secondary to acute infection).
Hyperglycemia (usually 300-600 mg/dL)

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30
Q

Macrovascular complications of diabetes

A

Atherosclerosis - related more to metabolic risk factors including obesity, dyslipidemia, arterial HTN rather than hyperglycemia

Manifestations:
- Coronary heart disease
- Cerebrovascular disease
- Peripheral artery disease
- Monckeberg arteriosclerosis
- Gangrene

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31
Q

Microvascular complications of diabetes

A

Diabetic nephropathy
Diabetic retinopathy, glaucoma
Diabetic neuropathy including diabetic gastroparesis
Diabetic foot

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32
Q

Pathophysiology of microvascular disease

A

Chronic hyperglycemia -> nonenzymatic glycation of proteins and lipids -> thickening of the basal membrane with progressive function impairment and tissue damage

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33
Q

What is a hormone?

A

Method by which cells in different parts of the body communicate
Chemical secreted into bloodstream by one set of cells and carried to another part of the body

34
Q

What is the effect of insulin on; muscle, liver, fat

A

Muscle: enhances glucose uptake, inhibits protein breakdown

Liver: inhibits gluconeogenesis

Fat: Increases lipogenesis

35
Q

Anterior pituitary hormones

A

‘Go Look For The Adenoma Please’

GH - Growth hormone - IGF-1
LH - leutenizing hormone
FSH - follicular stimulating hormone
- oestrogen/testosterone
TSH - T4, T3
ACTH - cortisol
Prolactin

36
Q

Where is testosterone produced in males and females

A

Males:
- Secreted by leydig cells 95%
- Adrenal steroids - peripheral conversion 5%

Females:
- Adrenal steroids - peripheral conversion 50%
- Ovarian 50%

37
Q

Posterior pituitary hormones and their actions

A

ADH - kidneys retain more water, reduce urine output, sudoriferous (sweat) glands decrease water loss by perspiration from skin, arterioles constrict which increases blood pressure

Oxytocin - uterine contractions, milk letdown

38
Q

Effect of exogenous testosterone on endogenous testosterone

A

Causes a decrease in endogenous testosterone (decreased GnRH, decreased LH, decreased testosterone, decreased FSH, decreased spermatogenesis)
It usually takes months for testicular testosterone production to recover

39
Q

fT4 and TSH levels for:
1. Primary hypothyroidism
2. Secondary hypothyroidism
3. Primary hyperthyroidism
4. Secondary hyperthyroidism

A
  1. fT4 reduced, TSH elevated
  2. fT4 reduced, normal or decreased TSH
  3. fT4 increased, TSH reduced
  4. fT4 increased, TSH normal or increased
40
Q

What is the test for hypocortisolism and how does it work?

A

Short synacthen test - test of secondary cortisol deficiency (ACTH deficiency)
- Test of adrenal gland function
- Synacthen is a polypeptide composed of the first 24 of 39 amino acids in ACTH
Stimulates cortisol production in the adrenal cortex
- Cortisol should increase to >450nmol/L 30-60 mins after synacthen (IV or IM)
- Cannot be used acutely as it takes >3 weeks to develop adrenal cortical atrophy

41
Q

What is the gold standard test for HPA function and how does it work? What are the limitations?

A

Insulin tolerance test:
- Cortisol and GH are counter-regulatory hormones that oppose insulin action to prevent hypoglycemia (secretion is stimulated by hypoglycemia)
- Administer actrapid insulin IV: 0.15 U/kg in most patients, 0.2-0.3 U/kg if insulin resistant or acromegaly
- ACTH deficiency: peak cortisol <500nmol/L
- Severe GH deficiency: Peak GH <3ng/ml
- aim for glucose nadir <2.2mmol/l, glucose can be administered orally or IV to correct hypoglycemia once glucose nadir achieved

Limitations:
- Hypoglycemia unpleasant for pt
- Small risk of LOC or seizure
- Resource intensive
- CI’d in patients w history of seizure, MI, arrhythmia

42
Q

What is the test for cushings syndrome and how does it work?

A

Cushings syndrome = hypercortisolism

1mg Dexamethasone suppression test
- Supraphysiologic dose of exogenous glucocorticoid, with long half life
- Take at 11pm, measure cortisol at 9am the next morning
- Normal response: cortisol falls to <50nmol/L, cushings syndrome: cortisol is not suppressed

43
Q

What is the test to diagnose primary hyperaldosteronism and how does it work?

A

Saline suppression test:
- Patient administered 2L normal saline over 4 hours
- Aldosterone measured at 0 and 4 hours
- Intact negative feedback: suppress aldosterone <170pmol/L
- Autonomous aldosterone production: aldosterone not suppressed

44
Q

Clinical features of primary aldosteronism

A

Causes up to 10% of severe hypertension
- bilateral adrenal hyperplasia
- Adrenal adenoma
- Elevated aldosterone to renin ratio suggests primary hyperaldosteronism

45
Q

Briefly describe aldosterone physiology

A

Aldosterone binds to the mineralocorticoid receptor to increase sodium retention in the distal nephron
- Aldosterone secretion is controlled by a complex set of negative feedback loops
- RAAS, hypokalemia, ACTH
- Renin is secreted by juxtaglomerular cells in glomerulus in response to hypovolemia
- If negative feedback is intact, volume expansion inhibits renin and consequently aldosterone secretion

46
Q

What causes normetaneprhine excess and how?

A

Phaeochromocytoma:
- Normetanephrine and metanephrine are metabolites of noradrenaline and adrenaline respectively
- Basal normetanephrine and metanephrine is a common screening test for phaeochromocytoma

Can also be caused by sympathetic nervous system overactivity

47
Q

How do you test for increased noradrenaline and adrenaline?

A

Clonidine suppression test
- Suppresses noradrenaline/normetanephrine production by SNS
- measure plasma normetanephrine before and 3 hrs after 300ug clonidine
- SNS overactivity: suppress plasma normetanephrine by >40% and into normal range
- Phaeochromocytoma: plasma normetanephrine doesn’t suppress

48
Q

What are the symptoms of a prolactinoma?

A
  • Bitemporal hemianopia (compression in macroprolactinoma (>10mm) - pain)
  • Headache
  • Galactorrhea, amenorrhea, vaginal dryness
  • Gynecomastia, erectile dysfunction
  • Decreased libido, infertility

Increased prolactin has negative feedback loop effect decreasing FSH, LH

49
Q

Causes of hypopituitarism:

A
  • Tumors
  • Haemorrhage/infarction - sheehans syndrome during pregnancy, increased demand for blood by pituitary cells + excessive blood loss during pregnancy, pituitary cells die, pituitary shrinks and scars
  • Accidental damage during radiation or surgery
50
Q

Impact of hypopituitarism on hormone secretion:

A

LH, FSH, GH lost before TSH, ACTH

51
Q

Symptoms of reduction in FSH and LH

A

In women:
- Oligomenorrhea, decreased menstrual bleeding
- Amenorrhea - absence of menstrual bleeding
- Infertility

In men:
- Loss of pubic hair
- Reduction in muscle mass

Sheehan’s syndrome:
- Absent menstruation
- Problems with postpartum lactation

52
Q

Symptoms of hypothyroidism:

A
  • Weight gain
  • Constipation
  • Hair loss
  • Low BP
53
Q

Symptoms of reduction in ACTH

A
  • Adrenal insufficiency: lack of cortisol production by adrenal glands
  • Weight loss
  • Delayed puberty
  • Low blood sugar and sodium levels
54
Q

Symptoms of reduction in growth hormone

A
  • Failure to grow (children)
  • Delayed puberty (in adolescents)
  • Decreased lean body mass
  • Low bone density
55
Q

What is cushings syndrome?

A

Endocrine disorder with elevated cortisol levels in the blood
Results from pituitary adenoma

56
Q

What are the effects of cortisol?

A

Maintains BP: Increases sensitivity of peripheral blood vessels to catecholamines, which narrows vessel lumen

Dampens inflammatory and immune response: decreased production of inflammatory mediators - prostaglandins and interleukins
Inhibiting T-Lymphocytes

57
Q

Cortisol response during stress:

A

Increased gluconeogenesis
Increased proteolysis - breakdown of protein
Increased lipolysis - breakdown of fat

58
Q

Regulation of cortisol

A

Cortisol levels peak in the morning, drop in the evening
Negative feedback decreases CRH and ACTH

59
Q

Causes of hypercortisolism

A

Pituitary adenoma - Cushings disease - excess ACTH
Tumors of adrenal gland - adenoma and carcinoma
Exogenous medications

60
Q

Clinical features of cushings syndrome

A

Cortisol levels are constantly higher than normal
- Central obesity
- Muscle skin and bone breakdown
- Elevated blood glucose levels and high insulin levels
- insulin targets adipocytes in centre of body and activates lipoprotein lipase

  • Buffalo hump
  • Moon shaped face
  • Easy bruising
  • Abdominal striae
  • Osteoporosis +/- fractures
61
Q

Diagnostic tests for cushings syndrome

A

Free cortisol 24hr urine sample
Free cortisol blood or saliva tests late at night
Dexamethasone suppression test

62
Q

Treatment for cushings disease

A

Cease exogenous medications
Surgical excision of pituitary adenoma
Adrenal steroid inhibitors - ketoconazole + metyrapone

63
Q

Imaging for suspected cushings syndrome

A

MRI of pituitary, CT of adrenals, CT of chest, abdomen or pelvis (ectopic site)

64
Q

What causes acromegaly?

A

Excess growth hormone (somatotropin)

65
Q

What increases growth hormone secretion physiologically?

A

Hypothalamus secretes GH releasing hormone every couple of hours, can increase with:
- Low blood glucose levels
- lack of food
- increased exercise
- increased sleep
- increased stress, trauma

66
Q

Direct effects of growth hormone

A

Organ growth
Increases insulin resistance

67
Q

Indirect effects of growth hormone

A

Stimulates certain tissues including liver, muscle, bone, kidneys
- Produce somatomedin C (Insulin like growth factor 1)
- Promotes cellular metabolism
- Helps cells divide and differentiate in body

68
Q

Clinical features of acromegaly

A

Growth of bones in hands, feet and lower jaw
Protrusion of forehead
Soft tissue swelling in hands, feet, face and tongue
Increased size of organs
Excess sweating

69
Q

Treatment of acromegaly

A

Somatostatin analogs - limit GH production
GH receptor antagonists

70
Q

Drug classes that are more likely to induce sustained hyperprolactinemia

A

Dopamine antagonists:
- Anti-psychotics
- Anti-depressants
- Anti-emetics

71
Q

Treatment of hyperprolactinemia

A

Dopamine agonists (cabergoline) as dopamine inhibits prolactin release

72
Q

Treatment for primary hypothyroidism

A

Thyroxine (oral)
Regular blood tests to monitor TSH levels

73
Q

Interpret the following TFTs:
TSH: 86mlU/L
fT4: 5pmol/L

A

Primary hypothyroidism

74
Q

Interpret the following TFTs:
TSH: <0.01mlU/L
fT4: 45 pmol/L

A

Primary hyperthyroidism

75
Q

Principles of diagnosing excess/reduced hormone levels

A

If suspect hormone is high, check when it should be low, vice versa
If too little, try to stimulate,
If too much, try to suppress

Testosterone, cortisol high in AM

76
Q

What happens in long-term corticosteroid use?

A
  • Adrenal glands stop making cortisol due to negative feedback
  • Eventually adrenal glands ‘go to sleep’ or atrophy
  • If long term corticosteroids are stopped suddenly, the adrenal gland does not immediately start making cortisol again, and adrenal crisis may ensue, which can be life threatening
77
Q

What is the purpose of a cortisol reserve?

A

Cortisol is critical to maintain BP during physiological stress (major illness, surgery)
- It is necessary to increase cortisol production during physiological stress

78
Q

Describe the basic physiology of diabetes insipidus

A

Diabetes insipidus can be due to:
- Lack of AVP secretion
- Kidney resistance to AVP

Arginine vasopressin (AVP) is stored and secreted by the posterior pituitary gland

AVP binds to AVP V2 receptor in distal nephron
- AVP secretion is stimulated by:
- Increase in plasma osmolality (hypothalamus)
- Hypovolemia (cardiac atria, carotid sinus, aortic arch)

  • Lack of AVP action causes thirst and hypotonic polyuria
79
Q

Diabetes insipidus diagnosis

A

Urine volume high
Weight >3% loss
Plasma Na >145mmol/L
Plasma osmolality >300 mosmo/kg
Urine osmolality <300 mosmo/kg

80
Q
A

General study MD3 (16 decks)

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