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Phase 2a > Endo > Flashcards

Endo Flashcards

1
Q

What is DMT1?

A

Disease of insulin deficiency caused by autoimmune destruction of beta-cells of the pancreas

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2
Q

Who does DMT1 usually effect?

A

Manifests in childhood/puberty and patient usually lean

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3
Q

What is LADA?

A

Latent autoimmune diabetes in adults. Slow burning variant with slower progression to insulin deficiency

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4
Q

Risk factors of DMT1

A

Northern European
Family history
Associated with other autoimmune diseases
Environmental Factors

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5
Q

What cells are destroyed in DMT1?

A

Autoimmune destruction by autoantibodies of Beta cells in the islets of Langerhans

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6
Q

What effect does insulin deficiency have on the liver?

A

Causes the continued breakdown of liver glycogen (producing glucose and ketones).

Leads to glycosuria and ketonuria as more glucose is in the blood

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7
Q

Effect of DMT1 in skeletal muscle and fats

A

There’s impaired glucose clearance which leads to an increased blood glucose.

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8
Q

At what mmol/L can the body no longer absorb glucose?

A

10mmmol/L - you become thirsty and get polyuria as the body is trying to remove excess glucose

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9
Q

What happens if T1 diabetics don’t have insulin?

A

Patients are prone to diabetic ketoacidosis

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10
Q

Why does DKA occur?

A

Reduced supply of glucose (as sig decline in circulating insulin) and increase in fatty acid oxidation (due to increase in circulating glucagon)

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11
Q

How does DKA lower the pH of blood?

A

Increased production of Acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidise them. Ketone bodies are v acidic so lower pH

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12
Q

Consequences of acidification of the blood?

A

Impairs the ability for Hb to bind to oxygen

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13
Q

Clinical sign of DKA

A

Breath smells like pear drops

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14
Q

What does complete Beta cells destruction result in?

A

Absence of serum C-peptide

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15
Q

DMT2 is a result of what?

A

Combination of insulin resistance and less severe insulin deficiency

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16
Q

Epidemiology of DMT2

A

All populations enjoying an affluent lifestyle
Older - >30
Overweight around the abdomen
South Asian, african, caribbean

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17
Q

Risk factors of DMT2

A 
Family history
Increasing age
Obesity and poor exercise
Ethnicity
Environment - low birth weight, poor-nutrition early
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18
Q

What other conditions is DMT2 associated with? (6)

A 
Central obesity
Hypertension
Hypertriglyceridemia
Decrease in HDL cholesterol
Disturbed homeostatic variables
Modest increase in pro-inflammatory markers
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19
Q

Tell me about insulin binding in DMT2

A

Binds normally to a receptor on the surface of cells - insulin resistance develops post-receptor

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20
Q

What are the levels of insulin in the blood like?

A

Circulating levels are higher due to hypersecretion by a depleted beta cell mass.

However, will begin to decline again after months or years due to secretory failure (starling curve of the pancreas)

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21
Q

What is IGT and IFG?

A

IGT - impaired glucose tolerance
IFG - impaired fasting glucose

Lifestyle changes can be made at these times to prevent DMT2

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22
Q

Acute presentation of young people with DMT1

A

Polyuria and nocturia - not enough glucose reabsorbed by kidneys which leads to more glucose in tubule urine and thus lots of water

Polydipsia - Loss of fluids and electrolytes which have to be replaced

Weight loss - fluid depletion and accelerated breakdown of fat and muscle

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23
Q

Complications of DM

A 
Staphylococcal skin infection
Retinopathy
Polyneuropathy
ED
Arterial disease resulting in MI or peripheral gangrene
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24
Q

What is acanthosis nigricans

A

Present in patients with severe insulin resistance - blackish pigmentation at the nape of the neck and axilla

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25
Q

DIagnostic ranges for DMT1 & 2

A

Random plasma glucose >11.1 mmol/L

Fasting plasma glucose > 7mmol/L

Borderline cases
OGTT
- Fasting >7
- 2hrs after glucose >11.1

HbA1c > 48mmol/mol

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26
Q

What other tests do you run to diagnose DM

A

Screen urine for microalbuminuria

FBC, U&Es, Liver biochem, Fasting blood sample for cholesterol and triglycerides

Blood pH to test for DKA

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27
Q

Diabetes can be secondary to what conditions?

A 
Pancreatitits
Trauma
Neoplasia of pancreas
Acromegaly
Cushing syndrome
Addisons
Drugs - Thiazide diuretics, Beta-blockers, immunosuppressives, Thyroid hormone
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28
Q

What is the MDT approach to DM treatment?

A

Education on disease and risks
Maintain lean weight, cease smoking and take care of feet
Encourage exercise
Low fat and sugar diet

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29
Q

Drug treatment for DMT1?

A

Synthetic human insulin via subcut injection
Short acting insulin given after a meal
Long acting insulin given before a meal

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30
Q

Complications of insulin treatment?

A

Hypoglycemia - most common
Injection site - lipohypertrophy
Insulin resistance
Weight gain - insulin makes people hungry

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31
Q

First line treatment of DMT2

A 
Lifestyle and dietary changes
Nutrient load spread throughout day
BP control - RAMIPRIL
Hyperlipidaemia control - STATINS
ORLISTAT - reduces fat absoprtion
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32
Q

Second line treatment of DMT2?

A

ORAL METFORMIN

  • reduces rate of gluconeogenesis
  • Increases cells sensitivity to insulin
  • helps with weight issue
  • Reduces CVD risk in diabetes

ORAL GLICLAZIDE

  • If metformin not working
  • promotes insulin secretion
  • ineffective in patients with no beta-cell mass
  • Avoided in pregnancy
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33
Q

Contraindications of metformin

A

Heart failure, liver disease or renal disease

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34
Q

What is hyperosmolar hyperglycaemic state?

A

Life threatening emergency characterised by marked hyperglycemia, hyperosmolality and mild or no ketosis

Characteristic of uncontrolled type 2 diabetes mellitus

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35
Q

RIsk factors for hyperosmolar hyperglycaemic state

A

Infection - most common cause, particularly pneumonia
Consumption of glucose rich fluids
Thiazide diuretics or steroids

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36
Q

Pathophysiology of hyperosmolar hyperglycaemic state

A

Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production

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37
Q

Presentation of hyperosmolar hyperglycaemic state

A 
Severe dehydration
Decreased levels of consciousness 
Hyperglycemia
Hyperosmolality
No ketones in blood or urine
Stupor or coma
Bicarb NOT LOWERED
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38
Q

Diagnosis of hyperosmolar hyperglycaemic state

A

Blood glucose > 11mmol/L
Urine stick testing shows heavy glycosuria
Plasma osmolality extremely high
Total body K+ low, serum K+ often raised due to absence of insulin which allows K+ to shift out of cells

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39
Q

Treatment of hyperosmolar hyperglycaemic state

A

Sensitive to insulin so lower rate of infusion
Fluid replacement
Low molecular weight heparin to reduce risk of thromboembolism, MI, stroke and arterial thrombosis
Restore K+ loss
Risk of cerebral oedema

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40
Q

Complications of diabetes

A

Reduced life expectancy
CV problems
CKD
Infections

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41
Q

Macrovascular complication of DM

A

Atherosclerosis which results in stroke, IHD and PVD

PVD can lead to lower limb amputation

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42
Q

Microvascular complications of DM

A 
Diabetic retinopathy
- leading cause of blindness in the world
- causes microaneurysms which can burst
Diabetic nephropathy
Diabetic neuropathy
Cataracts
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43
Q

Causes of hypoglycemia in diabetics?

A

Due to insulin or sulphonylurea treatment

E.g. increased activity, missed meal, accidental overdose

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44
Q

Cause of hypoglycemia in non-diabetics

A

EXPLAIN
EX - exogenous drugs - insulin, alcohol binge with no food
P - pituitary insufficency
L - liver failure
A - addison’s disease
I - Islets cell tumour & immune hypoglycemia
N - Non-pancreatic neoplasm

45
Q

Treatment of hypoglycemia

A

Oral sugar and long-acting starch (toast)

46
Q

What is the most common endocrine disorder?

A

Thyroid disease

47
Q

What TSH and (T3 & T4) levels would you expect in Hyperthyroidism?

A

TSH - Low

T3 & T4 - High

48
Q

What TSH and (T3 & T4) levels would you expect in Primary Hypothyroidism?

A

TSH - High

T3 & T4 - Low

49
Q

What TSH and (T3 & T4) levels would you expect in Secondary Hypothyroidism?

A

TSH - Low

T3 & T4 - Low

50
Q

Explain the TSH, T3 and T4 levels in hyperthyroidism?

A

Hyperthyroidism leads to more T3 and T4 being produced which suppresses TSH functions - So it’s low.

Exception is a pituitary adenoma which secretes TSH - so it’s high

51
Q

Explain the TSH, T3 and T4 levels in hypothyroidism?

A

Primary - TSH levels are high as it’s trying to stimulate more thyroid hormone release

Secondary (pituitary or hypothalamic) - TSH levels are low due to parts of the brain not working

52
Q

What is the pathophysiology of Graves disease?

A

Autoimmune condition where TSH receptor antibodies cause 1hyperthyroidism.

TSH receptor antibodies mimic TSH and stimulate TSH receptors on the thyroid

53
Q

What are the universal features of hyperthyroidism?

Imagine someone who’s extremely stressed

A 
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue Frequent loose Stools
Sexual dysfunction
54
Q

Unique features of Grave’s disease?

A

Exopthalmos - bulging of the eyeball due to inflammation and hypertrophy of the tissues behind the eyeball

Pretibial Myxoedema - deposits of mucin under the skin on anterior aspect of the leg. Gives a waxy, discoloured appearance

55
Q

What drugs do you give to treat hyperthyroidism>

A

First line - Carbimazole (usually succesful in treating graves disease)

Second line - Propylthiouracil

Radioactive iodine

Beta blockers to treat Adrenalin related symptoms

Surgery

56
Q

What is hashimoto’s thyroiditis and what is it associated with?

A

Most common cause of hypothyroidism in developed world

Autoimmune inflammation of the thyroid gland.

Associated with anti-TPO antibodies and immunoglobulin antibodies

Initially causes a goitre and then atrophy of the thyroid gland

57
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

58
Q

What else can cause hypothyroidism?

A

Hyperthyroidism treatments
Medications such as lithium
Central causes such as tumours, infection and radiation

59
Q

Presentation and features of hypothyroidism?

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention
Heavy/irregular periods
Constipation
60
Q

What is the management of hypothyroidism?

A

Replacement of thyroid hormone with levothyroxine

61
Q

What is levothyroxine?

A

Synthetic T4 which metabolises to T3 in the body

62
Q

What is Cushing’s syndrome?

A

Refers to signs and symptoms that develop after prolonged abnormal elevation of cortisol

63
Q

What is Cushing’s disease?

A

A specific condition where a pituitary adenoma secretes excessive ACTH

64
Q

Cushing’s syndrome features? (Round in the middle, thin limbs and high levels of stress hormone)

A 
Round moon face
Central obesity
Abdominal striae
Buffalo hump
Proximal limb muscle wasting
Hypertension
Cardiac hypertrophy
DMT2
Depression
Insomnia

Osteoporosis
Easily bruising and poor skin healing

65
Q

Causes of Cushing’s syndrome?

A

Exogenous steroids
Cushing’s diseases
Adrenal adenoma
Paraneoplastic Cushing’s

66
Q

What is paraneoplastic Cushing’s?

A

It’s when excess ACTH is released from a cancer and stimulates excessive cortisol release.

Most common is Small Cell Lung Cancer

67
Q

How to test whether someone has Cushing’s Syndrome?

A

Dexamethasone Suppression Tests (DST)

68
Q

Explain the Low Dose Dexamethasone Suppression Test

A

1mg of dexamethasone given at night and the levels of cortisol and ACTH are measured in the morning

Low cortisol –> normal
High/normal cortisol –> cushing’s syndrome

69
Q

Explain the High Dose Dexamethasone Test

A

8mg is given and it is used to work out the cause of the cushing’s syndrome

Low cortisol -> Cushing’s Disease

High/normal cortisol &
ACTH low -> Adrenal Cushings
ACTH high -> Ectopic ACTH

70
Q

Treatment for Cushings?

A

Surgical removal of tumour

71
Q

What is acromegaly?

A

The clinical manifestation of excessive growth hormone (GH)

72
Q

Where is GH produced?

A

Anterior pituitary gland

73
Q

Most common cause of unregulated GH secretion?

A

Pituitary adenoma

74
Q

What is GHRH?

A

Growth hormone releasing hormone - can be secreted by lung or pancreatic cancers (V rare)

75
Q

What happens if the pituitary adenoma grows too large?

A

Compresses the optic chiasm and leads to bitemporal hemianopia (loss of vision on outer half of both eyes)

76
Q

Presentation of acromegaly

A

Headaches
bitemporal hemianopia

Prominent forehead and brow
Large nose
Large tongue
Large hands and feet
Large protruding jaw
Arthritis

Hypertrophic heart
Hypertension
DMT2
Colorectal cancer

77
Q

Investigations for acromegaly

A

IGF-1 (raised)
Oral glucose tolerance test whilst measuring GH
MRI brain
Ophthalmology

78
Q

Treatment of acromegaly

A

Surgical removal of the cancer
Pegvisomant
Somatostatin analogues
Dopamine agonists

79
Q

What is Conn’s syndrome?

A

Also known as primary hyperaldosteronism.

It’s when the adrenal glands are directly responsible for producing too much aldosterone

80
Q

What affect does aldosterone have on the kidney?

A

+Na reabsorption from the distal tubule

+K secretion from distal tubule

+H secretion from collecting ducts

81
Q

What is the effect of aldosterone on the body?

A

Causes the BP to rise

82
Q

What effect does Conn’s have on serum renin levels

A

Serum renin will be low as it is suppressed by high BP

83
Q

What is secondary Hyperaldosteronism

A

It’s where excessive renin stimulating the adrenal glands causes more aldosterone to be produced

84
Q

Management of Hyperaldosteronism?

A

Aldosterone antagonists:
Eplerenone
Spironolactone

Treat underlying cause
Surgery

85
Q

Most common cause of secondary hypertension?

A

Hyperaldosteronism

86
Q

What is adrenal insufficency?

A

It’s when the adrenal glands don’t produce enough steroids; notable cortisol and aldosterone

87
Q

What is Addison’s disease?

A

Condition where the adrenal glands have been damaged resulting in a reduction of the secretion of cortisol and aldosterone.

Also called primary adrenal insufficiency

88
Q

Main cause of Addison’s?

A

Autoimmune

89
Q

What is secondary adrenal insufficency?

A

Inadequate Adrenocorticotropic hormone (ACTH) stimulating the adrenal glands resulting in low cortisol release

90
Q

What causes 2* adrenal insufficiency?

A

Result of loss or damage to the pituitary

91
Q

What is 3* adrenal insufficiency?

A

Inadequate release of Corticotropin releasing hormone (CRH) by the hypothalamus

92
Q

Usual cause of 3* adrenal insuffiency?

A

When the patient is on long term oral steroids and is suddenly taken off of them resulting in the hypothalamus not ‘waking up’ quickly enough

93
Q

Symptoms of adrenal insufficiency?

A 
Fatigue
Nausea
Cramps
Abdo pain 
Reduced libido
94
Q

Signs of adrenal insuffiency?

A

Bronze hyper-pigmentation of the skin

Hypotension

95
Q

What are the regions of the adrenal glands? Cortex and medulla

GFR - Makes Good Sex
(from outside in)

A

Zona glomerulosa - Mineralcorticoids (aldosterone)
Zona fasciculata - Glucocorticoids (cortisol)
Zona reticularis - Androgens

Medulla - secretes catecholamines (adrenaline and noradrenaline)

96
Q

Investigations for adrenal insuffiency?

A 
Hyponatraemia 
Hyperkalaemia
Early morning cortisol
*Short synACTHen test* - test of choice 
(ACTH high in 1* and low in 2*)
97
Q

Treatment of adrenal insufficiency?

A

Replacement steroids and electrolytes
Hydrocortisone replaces cortisol
Fludrocortisone replaces aldosterone

98
Q

What is diabetes insipidus (DI)

A

Lack of ADH or lack of response to ADH. This prevents the kidneys from being able to concentrate urine and leads to polyuria and polydipsia

99
Q

What are the two types of DI and explain them

A

Nephrogenic
- when the collecting ducts don’t respond to ADH

Cranial
- when the hypothalamus doesn’t produce ADH for the pituitary gland to secrete

100
Q

What causes each type of DI?

A

Nephrogenic

  • drugs, particularly lithium
  • Mutations in genes
  • Intrinsic kidney disease
  • Electrolyte disturbance

Cranial

  • Brain tumours
  • Brain malformations
  • Head injury
  • Brain infection
101
Q

Presentation of DI

A 
Polyuria
Polydipsia 
Dehydration
Postural hypotension
Hypernatreamia - water loss in excess of Na+ loss (Na becomes more concentrated)
102
Q

Investigation for DI

A

Water deprivation test
No fluids taken for 8 hours
Urine osmolality measured and synthetic ADH (desmopressin) administered
8 hrs later urine osmolality measured again

Cranial

  • After deprivation LOW
  • After ADH HIGH

Nephrogenic

  • After deprivation LOW
  • After ADH LOW

Primary Polydipsia

  • After deprivation High
  • After ADH HIGH
103
Q

Management of DI

A

Try and treat underlying cause

Desmopressin can be used

104
Q

What is Phaeochromocytoma

A

Tumour of the adrenaline-secreting chromaffin cells which causes an excess of adrenaline to be released.

Adrenaline is usually released in bursts giving periods of worse symptoms

Presentation - fight or flight response

105
Q

What is syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)

A

Excess ADH secretion due to the posterior pituitary or can be down to cancers such as small cell lung cancer

106
Q

Symptoms of SIADH

A 
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia - can cause seizures
107
Q

How does SIADH cause hyponatraemia?

A

Excess water reabsorption dilutes sodium in the blood and patients gets euvolaemic hyponatraemia

108
Q

Causes of SIADH (many)

A 
Post-op from major surgery
Infection
Head injury
Medications
Meningitis

Phase 2a (2 decks)

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