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Phase 2A conditions > Endocrine Conditions > Flashcards

Endocrine Conditions Flashcards

1
Q

What is the pathophysiology of type 1 diabetes mellitus?

A

Autoimmune pancreatic beta cell destruction - Destruction proceeds symptoms for years (insulitis) and at 80% destruction hyperglycaemia occurs: unable to utilise glucose and counter hormones are secreted leading to ketogenisis

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2
Q

What autoantibodies are involved in T1 diabetes?

A

insulin, islet-auto-antigen 2 and glutamic acid decarboxylase

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3
Q

What genes are involved in T1 diabetes?

A

HLA-DR/DQ polymorphism

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4
Q

What are risk factors for T1 diabetes?

A

Genetic predisposition, Infectious agents (may act as trigger), European

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5
Q

What symptoms does T1 diabetes present with and what values are to be expected?

A

hyperglycaemia (plasma glucose above 11.1) polyuria, polydipsia and weight loss

fasting glucose above 7, HbA1c 48 or higher, presence of ketones, little to no C-peptide

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6
Q

What tests should be ordered if T1 diabetes is suspected?

A

random plasma glucose, fasting plasma glucose and HbA1c (average blood glucose levels over the last 2 to 3 months)
Plasma or urine ketones and c-peptide

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7
Q

What are differentials for T1 diabetes?

A

T2 diabetes, monogenic diabetes (MODY)

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8
Q

What is MODY?

A

single gene mutation and responds to sulphonylureas such as gliclazide

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9
Q

What are some consequences of T1 diabetes?

A

ketoacidosis, neuropathy (commonly feet), renopathy, hyperglycaemic coma, CV disease

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10
Q

How do you treat T1 diabetes?

A

Basal-bolus insulin (i.e. determir + lispro), lifestyle modification, occasional metformin

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11
Q

What is a downside of tight glycemic control?

A

Very strict management can lead to hypoglycaemia (trade off)

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12
Q

what is Whipple’s triad?

A

Indicate hypoglycaemia

symptoms of low blood sugar, plasma glucose below 3 and symptoms resolved when corrected

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13
Q

What is the pathophysiology of type 2 diabetes mellitus?

A

progressive disorder: combination of impaired secretion and insulin resistance - starts off with resistance and compensatory mechanisms may lead to beta cell failure

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14
Q

What are some differences between T1 and T2 diabetes?

A

in T2 there is insulin detectable, which makes ketoacidosis and gluconeogenesis less likely. There is also no HLA link in T2.
T2 is more common.

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15
Q

What are risk factors for T2 diabetes?

A

older age, overweight, family history, stress, gestational diabetes

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16
Q

What symptoms does T2 diabetes present with and what values are to be expected?

A

Often starts asymptomatic and is caught in a screening: polyuria, polydipsia, skin infections, fatigue and blurred vision

fasting glucose above 7, Hb1Ac above 48, 2 hours after giving load glucose (75g oral glucose) glucose is above 11.1

High LDL can indicate dysplipidemia (same as high cholesterol or hyperlipidemia)

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17
Q

What tests should be ordered if T2 diabetes is suspected?

A

fasting glucose, HbA1c, OGTT (oral glucose tolerance test), random plasma glucose

lipid profile, urine ketones, c-peptide

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18
Q

What are differentials for T2 diabetes?

A

type 1 diabetes, gestational diabetes or pre-diabetes

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19
Q

What are some consequences of T2 diabetes?

A

similar to T1: ketoacidosis, CV conditions, hyperosmolar hyperglycaemic state (very high blood glucose levels)

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20
Q

How do you treat T2 diabetes?

A

initially with lifestyle changes and agree to a HbA1c target

Metformin, then dual therapy i.e. metformin and DPP4 inhibitor

If symptomatic consider insulin or sulfonylurea and review when control is achieved

in pregnancy give aspirin against preeclampsia

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21
Q

What is Diabetic ketoacidosis (DKA) and what is its pathophysiology?

A

Complication of diabetes: Hyperglycaemia, ketosis and acidosis
hyperglycaemia is caused by inefficient insulin production (worsened by up regulation of counter-regulatory hormones)
ketones from FFA are produced and end up in blood causing acidosis

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22
Q

What causes diabetic ketoacidosis?

A

mainly in T1 diabetes

infection, inadequate insulin treatment, drugs affecting carb metabolism,

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23
Q

How does DKA present?

A

nausea and vomiting, abdominal pain, dehydration, reduced consciousness, acetone smell on breath

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24
Q

What are the biochemical criteria for DKA?

A

hyperglycaemia (fasting glucose above 11), ketonanemia (above 3 or ketonuria) and blood pH below 7.3

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25
Q

What tests should be ordered if DKA is suspected?

A

venous blood gas, blood ketones, blood glucose, FBC

urinalysis, ECG to look for cardiac trigger

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26
Q

What are differentials of DKA?

A

HHS, lactic acidosis or starvation ketosis

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27
Q

What consequences does DKA have?

A

hypokalaemia, hypoglycaemia, brain injury

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28
Q

How do you treat DKA?

A
  • below 3.5 - IV fluids, potassium replacement and IV insulin
  • above 3.5 - IV fluids and IV insulin
  • If BP systole under 90 - fast fluid bolus otherwise just saline
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29
Q

when do you consider DKA to be resolved?

A

if blood pH is above 7.3, bicarbonate above 15 and ketones below 0.6

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30
Q

What is the pathology of Hyperosmolar hyperglycaemic state (HHS)?

A

Hyperglycaemia, hyperosmolality and volume depletion in the absence of ketoacidosis

results from relative insulin deficiency and up regulation of counter hormones - there is enough insulin to suppress lipolysis and therefore ketoacidosis
evolves over several days and leads to hypernatraemia

coupled with hyperglycaemia and inadequate water intake leads to hypovolaemia - a decline in eGFR aggravates this

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31
Q

what are differences between DKA and HHS?

A

HSS: slower onset, no ketones, increased mortality, some insulin present

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32
Q

What are some risk factors for HHS?

A

mostly T2, infection, postoperative, inadequate insulin, nursing home resident (more likely to be dehydrated)

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33
Q

How does HHS present?

A
  • Presents with cognitive impairment, polyuria, polydipsia, nausea, weakness and dry mucus membranes

elevated glucose (30+), no ketones, mild acidosis, serum osmolality above 320

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34
Q

What are differentials to HHS?

A

DKA, lactic acidosis or alcohol ketoacidosis

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35
Q

what tests do you order if you suspect HHS?

A

blood glucose, ketones, venous gases, serum osmolality, Glasgow coma scale, urinalysis

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36
Q

What are some consequences of HHS?

A

hypoglycaemia after treatment, coma, stroke, death

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37
Q

How do you treat HHS?

A

IV fluids and insulin and potentially replace potassium

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38
Q

what is the pathophysiology of hypothyroidism?

A

Underproduction of T3 and T4 (triiodothyronine and thyroxine)

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39
Q

what are the two types of hypothyroidism?

A

Primary and central (secondary and tertiary)

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40
Q

Define primary hypothyroidism and its aetiology

A

TSH above range and T4 below

autoimmune (Hashimotos), destruction of gland, drugs

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41
Q

Define central hypothyroidism and its aetiology

A

insufficient stimulation from TSH

  1. deficient synthesis and secretion
  2. biologically ineffective TSH

pituitary mass lesions, other tumours, infection, trauma, genetic defect

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42
Q

what are RF for primary hypothyroidism?

A

iodine deficiency, female, autoimune conditions, lithium use

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43
Q

What are the RF for central hypothyroidism?

A

TBI, radiation

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44
Q

What symptoms does hypothyroidism present with?

A

non specific symptoms such as lethargy and weakness, cold intolerance, weight gain, menstrual irregularities, myxoedema coma, non-pitting oedema

Primary may present with a goitre

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45
Q

What are some differentials of hypothyroidism?

A

depression and iodine deficiency

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46
Q

What tests would you order for hypothyroidism?

A

TSH and serum T4

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47
Q

What lab results would you expect in primary hypothyroidism?

A

elevated TSH and reduced T4

can have anti-TPO autoantibodies if hashimoto’s

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48
Q

What lab results would you expect in central hypothyroidism?

A

reduced T4 and normal or low TSH

MRI may reveal lesions

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49
Q

How do you treat hypothyroidism?

A

levothyroxine

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50
Q

What is the pathology of Grave’s disease?

A

Autoimmune thyroid condition associated with Hyperthyroidism

Infiltrating T-cells cause thyroid follicular cells to express HLA class 2 which causes an autoimmune cascade
TSH immunoglobulins bind to TSH receptors which stimulates T4
Negative feedback reduces TSH

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51
Q

What is the aetiology of grave’s disease?

A

TSH receptor antibodies,
genetics,
potentially alemtuzumab treatment

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52
Q

What are the risk factors for Grave’s disease?

A

female, 20-40 years old, HLA-DR3 polymorphism

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53
Q

What does Grave’s disease present with and what lab results would you expect?

A

heat intolerance, weight loss, diffuse goitre, orbitopathy (wide open eyes), myxoedema

decreased TSH, increased T3 and T4, TSH receptor antibodies present (TRAb)

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54
Q

What differentials are there for Grave’s disease?

A

toxic nodular goitre, gestational hyperthyroidism

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55
Q

What tests would you order if you suspect Grave’s disease?

A

TSH, TSH receptor antibody, T3 and T4

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56
Q

What are complications of Grave’s disease?

A

bone mineral loss, A.fib, congestive HF, thyroid storm

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57
Q

What is a thyroid storm and what does it present with?

A

Thyroid storm is untreated hyperthyroidism: tachycardia, fever, sweating, shaking and agitation

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58
Q

How do you treat a thyroid storm?

A

BB and reduce thyroid hormones: propylthiouracil

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59
Q

How do you treat Grave’s disease?

A

with antithyroid drugs (carbimazole)

surgery such as thyroidectomy or destroy gland with radioactive iodine

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60
Q

What is the pathology of Hashimoto’s thyroiditis?

A

Destruction of thyroid cells causing hypothyroidism

autoimmune mediated lymphocytic inflammation destroys the thyroid cells (thyroiditis), which causes release of T4 and transient hyperthyroidism - followed by hypothyroidism

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61
Q

what genes is Hashimoto’s associated with?

A

HLA-DR3 and DR5 genes

62
Q

What are the RF for Hashimoto’s?

A

female, postnatal period, autoimmune conditions and lithium therapy

63
Q

What does Hashimoto’s present with and what lab results would you expect?

A

cold intolerance, fatigue, dry skin, constipation and potentially an enlarged thyroid

TPO antibody positive, TRAb negative, low T3/T4, increased TSH

64
Q

What are differentials for Hashimoto’s?

A

Grave’s disease, toxic multi nodular goitre

65
Q

What tests would you order if you suspect Hashimoto’s?

A

TSH, T3+T4, TPO antibodies, TSH receptor antibodies , biopsy

66
Q

What consequences can Hashimoto’s have?

A

hyperlipidemia

67
Q

How do you treat Hashimoto’s?

A

levothyroxine

if symptoms are minimal then observe and monitor
if recurrent: ablation

68
Q

what are the four types of thyroid cancer?

A

papillary, follicular, medullary and anaplastic

69
Q

What are features of papillary thyroid cancer?

A

common, well differentiated and lymph node involvement

70
Q

What are features of medullary thyroid cancer?

A

originates in thyroid parafollicular C- cells, sporadic, produces calcitonin

71
Q

What are features of follicular thyroid cancer?

A

early forms are indolent then aggressive, direct haematogenous spread, hurtle cells

72
Q

What are features of anaplastic thyroid cancer?

A

undifferentiated, vascular invasion, can intrude on recurrent laryngeal nerve, worse survival

73
Q

What are RF of thyroid cancer?

A

head and neck radiation, female, family history

74
Q

How does thyroid cancer present?

A

palpable thyroid nodule and hoarseness of voice
normal TSH, biopsy can reveal what type of cancer
high calcitonin in medullary cancer

75
Q

What investigations would you order if you suspect thyroid cancer?

A

TSH, neck ultrasound, fine needle biopsy

serum calcitonin, T4+T3

76
Q

How do you treat thyroid cancer?

A

total thyroidectomy and levothyroxine

chemo for anapaestic types

77
Q

What are DPP-4 inhibitors used for and how do they work?

A

Gliptins: inhibit the action of the enzyme DPP-4 which normally destroys the hormone incretin. Increatin helps the body to produce more insulin

Prescribed as a secondary line in T2D

78
Q

Name some examples of DPP-4 inhibitors?

A

Alogliptin, Linagliptin and Sitagliptin

79
Q

What do you use levothyroxine for?

A

Replacing thyroid hormones in an underachieve thyroid or after thyroid ablation

80
Q

What do you use metformin for and how does it work?

A

Form of biguanide: lessens glucose absorption and makes body more sensitive to insulin

Type 2 diabetes (1st line) and sometimes T1D

81
Q

What are contraindications of metformin?

A

diabetic ketoacidosis, eGFR below 30, AKI, conditions that can cause hypoxia and hepatic insufficiency

82
Q

What enhances the effect of metformin?

A

Ace inhibitors

83
Q

What reduces the effect of metformin?

A

diuretics, oestrogen or corticosteriods

84
Q

What is Carbimazole and how does it work?

A

Antithyroid medication:
Carbimazole is a thionamide and reduces the amount of T4 released. It doesn’t affect T4 that has already been made but reduces further production - it therefore takes 4-6 weeks to work

85
Q

what is an alternative to carbimazole?

A

propylthiouracil which is also used in a thyroid storm

86
Q

What are the contraindications of carbimazole?

A

severe blood disorders

87
Q

What are SLGT-2 inhibitors and what are they used for?

A
  • Sodium-glucose co-transporter-2 inhibitors: reduce the amount of glucose absorbed into the kidney and reduce the amount of glucose in blood

prescribed for T2D

88
Q

What is a example of a SLGT-2inhibitor?

A

Dapagliflozin

89
Q

what are sulphonylureas and what are they used for?

A

Stimulate the pancreas to make more insulin

Prescribed in MODY and T2 diabetes (if hyperglycaemic with symptoms or if metformin is contraindicated )

90
Q

What are examples of sulphonylureas?

A

Glibenclamide or Gliclazide

91
Q

What is Cushing’s syndrome?

A

Clinical manifestation of hypercortisolism (any cause)

Manifestations result from excessive exposure to cortisol (includes exogenous cortisol i.e. steroids)

92
Q

What are the two types of Cushing’s syndrome?

A

ACTH dependent: high ACTH levels cause excess cortisol, Cushing’s disease (pituitary related such as adenoma), secreting tumours
ACTH independent: excess cortisol despite surpassed ACTH, adrenal adenoma

93
Q

What is Cushing’s disease?

A

pituitary related causes of Cushing’s syndrome

94
Q

What is the aetiology of Cushing’s syndrome?

A

corticosteroid treatment, ACTH-secreting pituitary adenomas

95
Q

How does Cushing’s syndrome present?

A

weight gain, dyslipidemia and glucose intolerance

more severe: facial plethora (swelling), increased subcutaneous fat, violaceous scarring and muscle weakness

96
Q

what are differentials of Cushing’s?

A

obesity and metabolic syndrome

97
Q

What lab results would you expect in someone with Cushing’s?

A

levated glucose, elevated cortisol, morning cortisol over 50 (dexamethasone suppression test)

98
Q

What tests would you order if you suspect Cushing’s?

A

erum glucose, late night salivary cortisol, dexamethasone suppression test (should suppress ACTH secretion and cortisol secretion), ACTH and imaging

99
Q

What are some consequences of cushing’s?

A

CV disease, HTN, diabetes and hypothyroidism

100
Q

How do you treat cushing’s?

A

Depends on the cause:
Cushing’s disease: transsphenoidal pituitary adenomectomy + Ketoconazale
Syndrome: Metyrapone for the management
Other: ablation of tumours or adrenalectomy

101
Q

what is acromegaly and what is the pathology?

A

Chronic disease caused by excessive secretion of growth hormone

Tumours can release GH causing and excess - passes through blood and leads to IGF-1 secretion by the liver
GF acts directly on organs and indirectly through IGF-1 causing uncontrolled growth

102
Q

What is the aetiology of acromegaly?

A

95% of cases are caused by pituitary adenomas, rarely endocrine tumours

(in 25% prolactin is co-secreted)

103
Q

What are RF for acromegaly?

A

GPR101 over expression, carney complex, family history

104
Q

How does acromegaly present?

A

coarse facial features (enlarged nose and jaw), macroglossia, soft tissue changes, carpal tunnel, joint pain

105
Q

what lab results would you expect in acromegaly?

A

elevated IGF-1, lack of surpassed GH during oral glucose test, elevated prolactin

106
Q

what is Pseudoacromegaly?

A

When IGF-1 is not elevated

107
Q

What tests would you order for acromegaly?

A

IGF-1, OGTT (GH should be low but since secretion in independent it remains high), pituitary MRI, prolactin

108
Q

Why is baseline serum GH not useful when testing for acromegaly?

A

baseline GH is not useful as it varies during the day (pulsatile release)

109
Q

What are some consequences of acromegaly?

A

cardiac problems, HTN, sleep apnoea, diabetes

110
Q

How do you treat acromegaly?

A

Treat depending on tumour:

pituitary: transphenoidal surgery and dopamine agonist (cabergoline)
unresectable: somatostatin (octreotide), dopamine agonist and debunking surgery
non-pituitary: somatostatin and surgery

111
Q

What is Conn’s syndrome and what is its pathology?

A

Primary aldosteronism: excessive aldosterone resulting in sodium reabsorption

Excessive aldosterone independent of angiotensin II causing excessive sodium reabsorption leading to hypertension and suppression of renin-angiotensin system

  • Potassium is lost
112
Q

What is the aetiology of conn’s syndrome?

A

genetics, adrenal adenomas

113
Q

How does conn’s syndrome present and what lab results would you expect?

A

hypertension, nocturia, polyuria, lethargy, mood disturbances, difficulty concentrating

in 20% potassium is low, aldosterone/renin ration above 20

114
Q

what are differentials of Conn’s syndrome?

A

HTN, thiazide induced hypokalaemia

115
Q

what tests would you order to test for conn’s syndrome?

A

plasma potassium, aldosterone/renin ratio, adrenal CT

116
Q

What are complications of Conn’s syndrome?

A

HTN, hypokalaemia, stroke, MI, HF, impaired renal function

117
Q

How do you treat Conn’s syndrome?

A

surgically removing adenoma or with a aldosterone antagonist (spironolactone)

118
Q

How does a pituitary adenoma form?

A

Hypermethylation of CDKI2A gene causes inactivation of it, leading to unregulated cell growth

119
Q

what are the two types of pituitary adenoma’s?

A

Functional: secreted hormones i.e. acromegaly or cushing’s disease

Non-functional (CNFPA): no hormone secretion, pituitary tumour transforming gene is over expressed in in CNFPA leading to cell growth and angiogenesis

120
Q

How do CNFPA’s present?

A

Symptoms are LT and progressive: headaches, erectile dysfunction, amenorrhea, infertility, fatigue, weight gain

121
Q

What labs would you order for a CNFPA and what results can you expect?

A

Order prolactin, contrast enhanced CT and exclude functional adenoma

elevated prolactin, anaemia and mass seen on CT and MRI

122
Q

what are consequences of CNFPA’s ?

A

diabetes insipidus, meningitis, hypopituitarism, pituitary apoplexy (bleeding into the pituitary)

123
Q

How do you treat CNFPA’s?

A

observing and if its near the optic chasm: surgery and hormone replacement

124
Q

what is Addison’s disease?

A

Destruction of the entire adrenal cortex resulting in aldosterone, cortisol and androgen deficiencies

125
Q

What causes Addison’s disease?

A

autoimmune adrenalitis, TB, metastases, LT steroid use, adrenal haemorrhage

126
Q

How does Addison’s present?

A

Presents with lethargy, depression, weight loss, vitiligo, bronzed skin, skin pigmentation, impotence, hypotension

127
Q

What tests would you order for Addison’s and what results would you expect?

A

abdominal CT, serum cortisol, serum ACTH, electrolytes

decreased serum cortisol, increased ACTH, increased renin, hyponatraemia, hyperkalaemia

128
Q

How do you treat Addison’s?

A

lifelong gluticocorticoid replacement

129
Q

How can you tell between Addison’s and secondary adrenal insufficiency?

A

secondary has no skin pigmentation, low ACTH and mineralocorticoid production intact

130
Q

What is SIADH?

A

syndrome of inappropriate ADH secretion: leading to an increase of water reabsorption, diluted blood leads to low sodium and less aldosterone to be released. This causes sodium to be excreted and water follows. We are now in a position where there is hyponatraemia.

131
Q

What are the four types of SIADH

A
  • Type A: erratic and independent of plasma osmolality, high ADH
  • Type B: constant release of ADH
  • Type C: baseline sodium concentration level is lower than normal
  • Type D: ADH is normal but still high urine osmolality
132
Q

what causes SIADH?

A

CNS disorders, ectopic ADH production (lung malignancies), medication, infection

133
Q

How does SIADH present and what lab results would you expect?

A

headache, nausea, vomiting, cramps, tremor, neurological symptoms as cells swell

low blood sodium levels, high urine sodium, low blood osmolarity

134
Q

How do you treat SIADH?

A

treat underlying cause and manage by restricting fluid intake and having a high salt diet
If severe: hypertonic UV fluids

135
Q

what is diabetes insipidus?

A

Disorder of fluid balance i.e. large volumes of dilute urine

136
Q

what are the two types of DI and their causes?

A

Neurogenic: caused by a decrease or absence of ADH
- idiopathic, congenital, genetic or damage to pituitary

Nephrogenic: Kidneys unresponsive to ADH secretion
- Causes include genetics, damage of renal tubules, lithium toxicity

137
Q

How does DI present?

A

polyuria, nocturia, dehydration, lack of other pituitary hormones

138
Q

what tests would you order to diagnose DI?

A

Cranial MRI, ADH levels, electrolytes, water deprivation test

139
Q

How does a water deprivation test separate neurogenic and nephrogenic causes of DI?

A

if urine osmolality increases it confirms neurogenic cause and if there is no increase it confirms nephrogenic causes

140
Q

How do you treat DI?

A

Treat depending on type:

- Neurogenic: desmopressin, chloropamide (increases renal response to low levels of ADH)
- Nephrogenic: NSAID’s, thiazide diuretics
141
Q

What value classifies hypokalaemia?

A

below 3.5

142
Q

How does hypokalaemia present?

A

mostly asymptomatic, if severe: constipation, muscle weakness, arrhythmia, polyuria

143
Q

What causes hypokalaemia?

A

increased kidney excretion, vomiting, diarrhoea, sweating, drugs, low dietary intake, insulin

144
Q

What can you see on an ECG in hypokalaemia?

A

flattened or inverted T waves, prolonged PR interval

145
Q

How do you treat hypokalaemia?

A

replenishing potassium and magnesium

146
Q

what classifies hyperkalaemia?

A

above 5.5.

147
Q

What causes hyperkalaemia?

A

decreased excretion, trans cellular shift (uncontrolled T1D, acidosis, massive cell lysis), increased intake

148
Q

How does hyperkalaemia present?

A

mostly asymptomatic, (remember MURDER) muscle weakness, urine, respiratory distress, decreased cardiac contractility, ECG changes, reflexes

149
Q

what changes are seen on an ECG in hyperkalaemia?

A

prolonged PR interval, peaked T waves, widened QRS interval

150
Q

How do you treat hyperkalaemia?

A

remember C BIG K DROP: calcium, beta 2 agonist, insulin and glucose, kayexalate (stops potassium from being absorbed), diuretics

Phase 2A conditions (7 decks)

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