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Osha 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is diabetes mellitus?

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia

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2
Q

What glucose levels define diabetes mellitus?

A
  • Symptoms and random plasma glucose > 11 mmol/l
  • Fasting plasma glucose > 7 mmol/l
  • No symptoms: OGTT (glucose tolerance) (75g glucose) fasting > 7mmol/l or 2h value > 11 mmol/l (repeated on 2 occasions)
    = HbA1c of > 48mmol/mol (6.5%)
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3
Q

How is carbohydrate metabolism regulated in non diabetics?

A
  • all glucose comes from liver (and a bit from kidney) either from breakdown of glycogen or gluconeogenesis
  • Glucose delivered to insulin independent tissues, brain and red blood cells
  • If insulin levels are low, muscle uses FFA for fuel
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4
Q

What happens to glucose after feeding?

A
  • Glucose stimulates insulin secretion and suppresses glucagon
  • 40% of ingested glucose goes to liver and 60% to periphery, mostly muscle
  • glucose replenishes glycogen stores in liver and muscle
  • High insulin and glucose levels suppress lipolysis and levels of non-esterified fatty acids (FFA) fall
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5
Q

What is the pathogenesis of T1DM?

A
  • insulin deficiency characterised by loss of β cells due to autoimmune destruction
  • may be triggered by viral infection
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6
Q

What is the pathophysiology of T1DM?

A
  • GLUT4 transporters require insulin to take up glucose from the blood and use it for fuel
  • no insulin produced so glucose remains in blood
  • cells think the body is being fasted so blood glucose levels keep rising causing hyperglycaemia
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7
Q

What are the risk factors for T1DM?

A
  • genetic predisposition
  • northern European
  • HLA DR3 or HLA DR4 human leukocyte antigens
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8
Q

What are some signs and symptoms of T1DM?

A
  • manifests in childhood and commonly presents with DKA
  • polyuria
  • polydypsia
  • sudden unexplained weight loss
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9
Q

Why is weight loss a sign/symptom of T1DM?

A
  • Excess fluid depletion and accelerated breakdown of fat and muscle due to insulin deficiency.
  • More common in T1DM as there is complete insulin deficiency so lipolysis and proteolysis occur more quickly
  • No glucose can enter cells in T1 but insulin is still produced in T2
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10
Q

What is the management of T1DM?

A
  • monitoring dietary carbohydrate intake and monitoring blood sugar levels
  • Subcutaneous insulin prescribed: background long acting insulin taken once a day and short acting insulin injected 30 mins before intake of carbs at meals
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11
Q

What are the criteria for DKA?

A
  • ketoacidosis: blood ketones > 3mmol/l
  • hyperglycaemia: blood glucose > 11mmol/l
  • acidosis pH < 7.3
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12
Q

What is the aetiology of DKA?

A
  • untreated/undiagnosed T1DM
  • infection/illness
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13
Q

What is ketoacidosis?

A

uncontrolled catabolism associated with insulin deficiency

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14
Q

What is the pathophysiology of DKA?

A
  • Insulin absence > unrestrained gluconeogenesis and dec peripheral glucose uptake > hyperglycaemia as higher blood glucose
  • Hyperglycemia > osmotic diuresis > more water in urine > dehydration and electrolyte loss
  • Peripheral lipolysis for energy > inc in circulating FFAs > oxidised to Acetyl CoA > ketone bodies (acidic) = Acidosis
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15
Q

How does DKA present?

A
  • Nausea + Vomiting
  • dehydration > can cause hypotension
  • Abdominal pain
  • acetone breath smell
  • lethargy
  • respiratory compensation for acidosis leading to hyperventilation (Kussmaul breathing)
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16
Q

Why is insulin treatment for DKA dangerous?

A
  • Insulin decreases blood potassium levels by redistributing K+ via the sodium-potassium pump
  • this causes low serum K+ leading to hypokalaemia
  • can lead to arrhythmia, weakness
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17
Q

How is DKA diagnosed?

A
  • recognised from the clinical features
  • confirmed by blood glucose and ABG
  • U&E: raised due to dehydration
  • urine dipstick - glycosuria and ketonuria
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18
Q

How is DKA managed?

A
  • ABC if unconscious
  • fluid loss replaced with IV 0.9% saline
  • give insulin and glucose (inhibits gluconeogenesis and therefore ketone production
  • restore electrolytes
  • treat underlying triggers e.g. infection
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19
Q

What is a possible complication of DKA and why?

A
  • cerebral oedema
  • the blood is initially very concentrated with high salt levels and is rapidly diluted
  • osmotic shifts occur and water moves from the blood into tissues
  • causes swelling of the brain
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20
Q

What is the definition of type 2 diabetes?

A

A progressive disorder characterised by inc insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors

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21
Q

What is the aetiology of type 2 diabetes?

A
  • age
  • obesity
  • family history
  • genetics: determines whether or not you develop the disease, lifestyle factors determine when. genetic link stronger than in T1DM
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22
Q

What is the epidemiology of type 2 diabetes?

A

Mainly found in Asians, men, elderly. Mostly in over 40s but prevalence increasing in teenagers

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23
Q

What are the risk factors for type 2 diabetes?

A

smoking, obesity, hypertension, sedentary lifestyle, age, ethnicity, family history

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24
Q

What is the pathophysiology of type 2 diabetes?

A
  • Repeated exposure to glucose and insulin leads to insulin resistance > more insulin needed to produce response from cells for glucose uptake.
  • β cells become fatigued and damaged > produce less insulin
  • insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia
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25
Q

What are the signs and symptoms of T2DM?

A
  • polyuria
  • polydypsia
  • opportunistic infection
  • slow healing
  • lethargy
  • glucose in urine (glycosuria)
  • blurred vision
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26
Q

Why are polyuria and glycosuria symptoms of diabetes?

A
  • glucose draws water into the blood by osmotic diuresis
  • high levels of glucose in the blood and not enough glucose can be reabsorbed as kidneys have reached the renal maximum reabsorptive capacity of glucose.
  • leads to excessive levels of glucose and water being excreted
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27
Q

What are the microvascular complications associated with diabetes?

A
  • diabetic retinopathy > visual loss,
  • nephropathy > end stage renal disease
  • neuropathy > foot ulcers and amputation
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28
Q

What are the macrovascular complications associated with diabetes?

A
  • stroke
  • CVD/MI
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29
Q

What is the gold standard test for T2DM?

A
  • HbA1c test > tells average blood glucose levels over the past 3 months
  • > 48mmol/mol = diabetes
  • > 42-47 mmol/mol= pre-diabetes
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30
Q

What is 1st line management for T2DM?

A
  • dietary changes, higher in complex carbs, low in fat and sugar
  • smoking cessation and dec alcohol
  • inc exercise
  • blood glucose and HbA1c monitoring
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31
Q

What is 2nd line management for T2DM?

A
  • metformin: inc insulin sensitivity
  • if HbA1c remains high then add in either:
    DPP4 inhibitor, sulphonylurea or thiazolidinedione
  • if still high then add in insulin
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32
Q

What is the action of metformin?

A
  • inc peripheral insulin sensitivity, decreases liver production of glucose
  • reduces insulin resistance by modifying the glucose metabolic pathways
  • lowers blood glucose levels
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33
Q

What is the action of sulphonylureas?

A
  • stimulate insulin release by binding to β cell receptors
  • don’t prevent failure of insulin secretion and can cause hypoglycaemia
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34
Q

What is the action of thiazolidinediones?

A
  • activate genes concerned with glucose uptake, utilisation and lipid metabolism
  • improve insulin sensitivity but need insulin for a therapeutic effect
  • can inc weight, risk of heart failure and fractures
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35
Q

Describe the pathogenesis of acromegaly

A
  • Commonly caused by excess release of growth hormone from pituitary tumour
  • GH binds to receptor in liver causing release of insulin-like growth factor 1 (IGF-1)
  • IGF-1 stimulates soft tissue and skeletal overgrowth
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36
Q

What is the relationship between IGF-1, somatostatin and GH?

A

IGF-1 stimulates the release of somatostatin which inhibits GH production from the hypothalamus

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37
Q

What are some signs of acromegaly?

A
  • prominent forehead and brow
  • large hands, nose, feet, tongue
  • bitemporal hemianopia (pressure on optic chiasm)
  • profuse sweating
  • larger jaw
  • wide spaced teeth
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38
Q

What are some symptoms of acromegaly?

A
  • headaches
  • arthritis due to bony overgrowth
  • fatigue
  • carpal tunnel syndrome
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39
Q

What is the gold standard investigation for acromegaly?

A

OGTT: normally GH is inhibited by a rise in glucose, so should be undetectable but GH release is unsuppressed in acromegaly

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40
Q

What is the 1st line investigation for acromegaly?

A

IGF-1 test, levels will be increased correlating with increased levels of GH

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41
Q

What is the management of acromegaly?

A
  • surgical removal of pituitary adenoma via transsphenoidal surgery
  • if surgery isn’t appropriate then:
  • somatostatin analogues to block GH release
  • GH receptor antagonists
  • dopamine agonists which suppress GH
  • radiotherapy
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42
Q

What are common complications of acromegaly?

A
  • insulin resistant diabetes
  • htn and heart disease
  • cerebrovascular events
  • arthritis
  • sleep apnoea
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43
Q

What is hypothyroidism?

A

A clinical syndrome resulting from the deficiency of thyroid hormones resulting in a slowing of metabolic processes

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44
Q

What is the epidemiology of hypothyroidism?

A
  • way more common in women than men
  • mean age of diagnosis around 60
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45
Q

What is the aetiology of hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • iodine deficiency
  • medications for hyperthyroidism (carbimazole)
  • lithium and amiodarone
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46
Q

Describe the pathophysiology of Hashimoto’s thyroiditis

A
  • autoimmune destruction by cell and antibody mediated processes
  • formation of antithyroglobulin and antithyroid peroxidase (anti-TPO) antibodies that attack the thyroid tissue causing progressive fibrosis
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47
Q

Describe the pathophysiology of hypothyroidism

A
  • 1º hypothyroidism: in peripheral thyroid disorder, T3 or T4 isn’t produced and to compensate, TSH levels rise
  • 2º hypothyroidism: pituitary disorder causes decreased TSH levels which leads to lowered T3/T4 levels
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48
Q

Describe the presentation of hypothyroidism

A
  • Weight gain
  • Depression/low mood
  • Menstrual disturbance
  • Fatigue
  • Muscle cramps
  • Cold intolerance

Presentation
- bradycardia
- goitre
- slow reflexes

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49
Q

What investigations are done for hypothyroidism, what are the relevant TSH, T3 & T4 levels and where does the problem lie according to these levels?

A
  • thyroid function tests (TFTs)
  • High TSH and Low T3/T4 = 1º hypothyroidism = thyroid
  • Low TSH and Low T3/T4 = 2º hypothyroidism = pituitary
  • can check for elevated TPO levels indicating autoimmunity
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50
Q

How is hypothyroidism managed?

A
  • Replacement of thyroid hormone by levothyroxine
  • is synthetic T4 that metabolises to T3 in the body
  • If TSH is too low then the dose needs to be increased and vice versa
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51
Q

What is the difference between hyperthyroidism and thyrotoxicosis?

A
  • hyperthyroidism: overproduction of thyroid hormone by the thyroid gland
  • thyrotoxicosis: excessive T3 + T4 in circulation
52
Q

Describe the aetiology of hyperthyroidism

A
  • Grave’s disease
  • iodine excess
  • toxic multinodular goitre
  • thyroiditis
53
Q

Describe the pathophysiology of hyperthyroidism

A
  • High T3 AND T4, low TSH
  • 1º: thyroid producing excess thyroid hormone
  • 2º: thyroid producing excess due to overstimulation by TSH - pathology in hypothalamus or pituitary
54
Q

How does hyperthyroidism present?

A
  • Weight loss
  • feverish
  • tachycardia
  • anxiety
  • heat intolerance
  • diarrhoea (inc bowel metabolism)
  • menstrual disturbance
  • everything increases
55
Q

How is hyperthyroidism managed?

A
  • 1st line: anti-thyroid drug: carbimazole
  • 2nd line: propylthiouracil
  • radioiodine therapy: radioactivity destroys thyroid cells
  • β blockers
  • surgery
56
Q

What is Grave’s Disease?

A
  • autoimmune condition
  • TSH receptor antibodies cause primary hyperthyroidism
  • abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid
57
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A
  • Cushing’s syndrome: signs and symptoms which develop after prolonged, abnormal elevation of cortisol
  • Cushing’s disease: a pituitary adenoma secretes excessive ACTH
  • Cushing’s disease can cause Cushing’s syndrome but the syndrome isn’t always caused by the disease
58
Q

What is the aetiology + epidemiology of Cushing’s?

A
  • ACTH independent: iatrogenic e.g. steroids (most common) or adrenal adenoma
    ACTH dependent: Cushing’s disease (most common dependent) or ectopic ACTH (small cell lung/neuroendocrine tumour
  • more likely in women
59
Q

What is the presentation of Cushing’s?

A
  • round moon face
  • central obesity
  • abdominal striae
  • proximal limb muscle wasting
  • fat pad on upper back
  • hypertension
  • hyperglycaemia
  • depression
  • insomnia
60
Q

What is the investigation of Cushing’s?

A
  • 1st line: raised plasma cortisol
  • CT/MRI for tumours
  • Low dose dexamethasone test initially
61
Q

What is the low dose dexamethasone test?

A
  • patient takes 1mg at night and cortisol and ACTH are measured in the morning
  • normal: dexamethasone suppresses cortisol release by -ve feedback on hypothalamus and pituitary
  • hypothalamus reduces CRH, pituitary reduces ACTH
  • Cushing’s: cortisol not suppressed
62
Q

What is high dose dexamethasone test?

A
  • 8mg dexamethasone
  • low cortisol: Cushing’s disease
  • High cortisol, low ACTH: Adrenal Cushing’s
  • High cortisol, high ACTH: ectopic ACTH
63
Q

What is the management of Cushing’s?

A
  • transsphenoidal removal of pituitary adenoma
  • surgical removal of adrenal tumour or tumour producing ectopic ACTH
  • iatrogenic: stop steroids
64
Q

What is primary adrenal insufficiency and what is it caused by?

A
  • Also called Addison’s disease
  • adrenal glands are damaged
  • cortisol and aldosterone production impaired
  • autoimmune or caused by TB
65
Q

What is secondary adrenal insufficiency and what is it caused by?

A
  • damage to or loss of the pituitary gland
  • inadequate ACTH stimulating adrenals
  • leads to low cortisol release
66
Q

What is tertiary adrenal insufficiency and what is it caused by?

A
  • results from inadequate CRH release from the hypothalamus
  • iatrogenic: long term use of steroids (+ 3 weeks) > hypothalamus suppression
  • sudden steroid withdrawal doesn’t allow hypothalamus to regain normal functioning
67
Q

How does adrenal insufficiency present?

A
  • Fatigue
  • Vitiligo
  • Abdo pain + nausea
  • postural hypotension (dec aldosterone)
  • hyperpigmentation
68
Q

In which type of adrenal insufficiency does hyperpigmentation present and why?

A
  • In primary
  • ACTH stimulates melanocytes to produce melanin
  • hyperpigmentation seen in palmar creases
69
Q

How is Addison’s investigated?

A
  • Gold standard: Short synacthen: give patient synacthen (synthetic ACTH) in morning (9am)
  • failure of cortisol to rise after 30 mins indicates Addison’s
  • U&E > hyponatraemia, hyperkalaemia,
  • low glucose
70
Q

How is Addison’s managed?

A
  • hydrocortisone to replace cortisol
  • fludrocortisone to replace aldosterone > inc Na and dec K to correct postural hypotension
  • double dose in acute illness for stress response
71
Q

What is SIADH?

A
  • syndrome of inappropriate ADH
  • condition where there are inappropriately large amounts of ADH
72
Q

What is the pathophysiology behind SIADH?

A
  • ADH produced in hypothalamus and secreted by posterior pituitary
  • Stimulates water reabsorption in collecting ducts
  • water dilutes sodium > hyponatraemia
  • leads to euvolaemic hyponatraemia (normal body sodium, inc in total body water)
  • patients have high urine osmolality and high urine sodium
73
Q

What is the aetiology of SIADH?

A
  • iatrogenic: post operative/medication (SSRIs, NSAIDs, carbamazepine)
  • infection e.g. pneumonia, lung abcess
  • head injury
  • meningitis
  • ectopic production of ADH e.g. from small cell lung
74
Q

How does SIADH present?

A
  • nausea + vomiting
  • headache
  • fatigue
  • muscle aches and cramps
  • confusion
  • mild/severe hyponatraemia (115-125/<115mmol/L)
75
Q

How is SIADH investigated?

A
  • diagnosis of exclusion
  • clinical exam: euvolaemia
  • U&E: hyponatraemia
  • urine sodium and osmolality: high
  • serum osmolality: low
76
Q

How is SIADH managed?

A
  • stop the cause (if meds)
  • fluid restriction: 0.5-1L
  • Tolvaptan: ADH receptor blocker > causes inc in sodium levels
77
Q

What is nephrogenic diabetes insipidus and what are some causes?

A
  • Collecting ducts don’t respond to ADH
  • lithium
  • mutations in gene coding for ADH receptor
  • electrolyte disturbance
78
Q

What is diabetes insipidus?

A
  • lack of ADH (cranial) or lack of response to ADH (nephrogenic)
  • prevents kidneys being able to concentrate urine > polyuria or polydipsia
79
Q

What is cranial diabetes insipidus and what are some causes?

A
  • hypothalamus doesn’t produce ADH
  • idiopathic
  • brain tumour, infection, surgery, head injury
80
Q

How does diabetes insipidus present?

A
  • polyuria
  • polydipsia
  • dehydration
  • postural hypotension (BP drops on standing after sitting/lying down)
  • hypernatraemia
  • nocturia: waking in night to urinate
81
Q

How is diabetes insipidus investigated?

A
  • low urine osmolality
  • high serum osmolality
  • water deprivation test (gold standard)
82
Q

What is the water deprivation test?

A
  • patient avoids taking in fluids for 8hrs
  • urine osmolality measured and desmopressin administered
  • urine osmolality measured 8hrs later
  • in CDI > urine osmolality: low > high
  • in NDI > urine osmolality: low > low
83
Q

How is diabetes insipidus managed?

A
  • treat underlying cause
  • desmopressin (synthetic ADH)
84
Q

What is prolactinoma?

A
  • lactotrophs in anterior pituitary produce and release prolactin
  • type of pituitary adenoma
  • presents most in biological females aged 20-40
85
Q

What is the pathophysiology of prolactinoma?

A
  • hypersecretion of prolactin causes secondary hypogonadism > due to inhibitory effects on GnRH
86
Q

How does prolactinoma present in females and why?

A
  • decreased release of GnRH > decrease in LH and FSH > decrease in oestrogen and progesterone
  • amenorrhoea or oligomenorrhoea
  • infertility
  • galactorrhoea
  • low libido
87
Q

How does prolactinoma present in males and why?

A
  • decreased release of GnRH > decreased testosterone
  • low testosterone
  • erectile dysfunction
  • reduced facial hair
  • low libido
  • can have galactorrhoea
88
Q

How is prolactinoma investigated?

A
  • serum prolactin levels
  • pituitary MRI to detect adenoma
89
Q

How is prolactinoma managed?

A
  • 1st line: dopamine agonists e.g. oral bromocriptine
  • dopamine inhibits prolactin and shrinks the prolactinoma
  • 2nd line: HRT e.g. oestrogen (if fertility and galactorrhoea aren’t issues
90
Q

What is Conn’s syndrome?

A
  • primary hyperaldosteronism
  • excess of aldosterone
  • serum renin is low as it is suppressed by high bp
91
Q

What is the aetiology of primary hyperaldosteronism?

A
  • Adrenal adenoma (only actual cause of Conn’s, others are hyperaldosteronism)
  • bilateral adrenal hyperplasia
92
Q

What is secondary hyperaldosteronism and its aetiology?

A
  • excessive renin stimulating adrenal glands to produce more aldosterone
  • serum renin is high
  • renal artery stenosis/obstruction
  • heart failure
93
Q

How does Conn’s present?

A
  • often asymptomatic
  • hypertension (Conn’s + hyperaldosteronism are usually indistinguishable unless measuring renin + aldosterone)
  • headaches
  • hypokalaemia (excretion of K+)
  • weakness, cramps, polyuria, polydipsia, thirst
94
Q

How is Conn’s investigated?

A
  • high aldosterone, low renin = 1º
  • high aldosterone, high renin = 2º
  • CT/MRI to look for adrenal mass
  • selective adrenal venous sampling (gold)
95
Q

How is Conn’s managed?

A
  • aldosterone antagonists to control BP and low K+ e.g. Spironolactone
  • adrenalectomy
  • percutaneous renal artery angioplasty for 2º hyperaldosteronism
96
Q

What is the physiology of the parathyroid?

A
  • 4 parathyroid glands
  • chief cells produce PTH
  • PTH increases serum Ca by:
  • inc osteoclast activity, Ca reabsorption in kidney, vit D activity > more Ca absorbed in intestines
97
Q

What is primary hyperparathyroidism?

A
  • uncontrolled parathyroid hormone produced by a tumour of the parathyroid gland
  • leads to hypercalcaemia
  • treated by surgical removal of the tumour
98
Q

What is secondary hyperparathyroidism?

A
  • insufficient vitamin D or chronic renal failure leads to low calcium absorption
  • causes hypocalcaemia
  • more PTH excreted in response to low serum calcium
  • leads to hyperplasia of glands
  • therefore, low/normal serum calcium and high PTH
  • management: treat vit D deficiency/renal transplant
99
Q

What is tertiary hyperparathyroidism?

A
  • 2º continues for a long time
  • hyperplasia of glands so PTH baseline increases dramatically
  • PTH levels remain high even after 2º is treated
  • high PTH and absent previous pathology > high calcium absorption + hypercalcaemia
  • treated by surgical removal of PTH tissue
100
Q

What is the presentation of hyperparathyroidism?

A
  • hypercalcaemia: stones, bones, groans, moans
  • renal stones
  • painful bones
  • groans: constipation, nausea, vomiting
  • moans: fatigue, depression, psychosis
101
Q

How is hyperparathyroidism investigated?

A
  • bones: DEXA scan for osteoporosis
  • stones: ultrasound
  • groans: abdo X-ray
  • moans: radioisotope scanning for adenoma
102
Q

What is hypokalaemia and how is it caused?

A
  • low serum potassium
  • dec potassium intake, dec entry into cells, inc excretion through sweat, urine, GI, hyperaldosteronism
103
Q

What is the hyperosmolar hyperglycaemic state (diagnosis criteria)?

A
  • life-threatening emergency characterised by:
  • hyperglycaemia: ≥30mmol/L
  • hyperosmolality: ≥320mOsm/kg (due to inc serum glucose and potassium
  • no ketoacidosis
104
Q

What is the pathophysiology behind hyperosmolar hyperglycaemic state?

A
  • some insulin still produced by pancreas
  • sufficient to inhibit hepatic ketogenesis (preventing ketogenesis)
  • insufficient to inhibit hepatic glucose prod
  • leads to osmotic diuresis, loss of Na and K
  • hyper viscosity of blood + volume depletion
105
Q

What is the presentation of the hyperosmolar hyperglycaemic state?

A
  • dehydration, polyuria, polydypsia
  • lethargy, nausea, vomiting
  • altered level of consciousness (low GCS)
  • focal neurological deficits
  • hyperviscoscity
106
Q

How is the hyperosmolar hyperglycaemia state managed?

A
  • fluid replacement: IV 0.9% NaCl solution
  • insulin: should NOT be given unless blood glucose falls while giving IV fluids
  • venous thromboembolism prophylaxis
107
Q

What is pheochromocytoma?

A
  • neuroendocrine tumour of the chromatin cells in the medulla of the adrenal glands
  • secretes large quantities of the catecholamine hormones noradrenaline and adrenaline
  • stimulates the SNS and fight or flight response
108
Q

What is the presentation of pheochromocytoma?

A
  • anxiety
  • sweating
  • headache
  • htn
  • palpitations, tachycardia, paroxysmal AF
109
Q

How is pheochromocytoma diagnosed and managed?

A
  • 24hr urine catecholamines
  • plasma free metanephrines: breakdown product of adrenaline with a longer half life
  • α blockers first (phenoxybenzamine), β blockers, surgical management is definitive
110
Q

What are the causes and pathophysiology behind hyperkalaemia?

A
  • Causes: AKI, spironolactone, Addison’s, DKA
  • inc K+ decreases action potential threshold leading to easier depolarisation and abnormal heart rhythms
111
Q

How is hyperkalaemia diagnosed?

A
  • high K+ on U&Es
  • serum potassium >5.5mmol/L
  • ECG: absent P wave, prolonged PR interval, tall T waves, widened QRS complex
112
Q

How is hyperkalaemia treated?

A
  • urgent: calcium gluconate to stabilise the cardiac membrane then insulin and dextrose
113
Q

What are differential diagnoses for hyperkalaemia?

A
  • CKD, DKA, HHS
  • uncommon: AKI, Addison’s
114
Q

How is hypoparathyroidism diagnosed and treated?

A
  • decreased PTH, decreased Ca2+, inc phosphate and long QT
  • treatment: calcium supplements and vit D3
115
Q

What is the presentation of hypoparathyroidism/hypocalaemia?

A
  • Cats go numb: convulsions, arrhythmias, tetany (involuntary muscle contraction), numbness in hands, feet and around mouth
  • Chvostek’s sign: facial spasm when tapping over CN7
  • Trousseau’s sign: carpopedal spasm
  • calcium <8.5mg/dL
116
Q

What are the causes of hypoparathyroidism?

A
  • 1º: DiGeorge and idiopathic
  • 2º: surgical
117
Q

What is the role of ghrelin?

A
  • stimulates hunger
  • produced by P/D1 cells in stomach and epsilon cells in pancreas
  • levels inc before meals and dec after meals
118
Q

What is the role of leptin?

A
  • regulates body weight
  • produced by adipose tissue so more adipose = more leptin
  • acts on satiety centres in hypothalamus and decreases appetite
  • stimulates release of melanocyte-stimulating hormone and CRH
119
Q

How is obesity managed?

A
  • conservative: diet + exercise
  • Orlistat: pancreatic lipase inhibitor
  • Liraglutide: glucagon-like peptide-1 (GLP-1) used in T2DM
120
Q

How is hypercalcaemia managed?

A
  • rehydration with saline and bisphosphonates
  • calcitonin
  • steroids if sarcoidosis
121
Q

What is the cause of hypercalcaemia?

A
  • primary hyperparathyroidism
  • malignancy: PTHrP from tumours, bone metastases or myeloma
  • sarcoidosis, acromegaly, thyrotoxicosis
122
Q

What is the definition of hypoglycaemia?

A
  • glucose below the normal fasting glucose levels
  • blood glucose levels below 3 mmol/L
123
Q

What is the pathophysiology behind hypoglycaemia?

A
  • when glucose is taken up by cells, blood glucose levels drop
  • this stimulates α islet cells to produce glucagon and reduces the production of insulin
  • glucagon increases liver gluconeogenesis and glycogenolysis
  • production of adrenaline, GH, cortisol
  • interruption of one or more mechanisms causes hypoglycaemia
124
Q

What are the symptoms of hypoglycaemia?

A
  • sweating, shaking, hunger, anxiety, nausea
  • weakness, vision changes, confusion, dizziness
125
Q

How is hypoglycaemia treated?

A
  • oral glucose
  • IM/SC injection of glucagon
  • IV 20% glucose solution last resort hospital setting
126
Q

What is De Quervain’s thyroiditis?

A
  • subacute granulomatous thyroiditis
  • occurs post viral infection
  • presents with hyperthyroidism
  • treated with NSAIDs

Osha 2a (15 decks)

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