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Jack Misc List > Endocrinology list conditions (red and orange) > Flashcards

Endocrinology list conditions (red and orange) Flashcards

1
Q 
Hyperthyroidism (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. An excess of thyroid hormones in the blood.
  2. 75% are caused by Graves’ disease. Other causes are Toxic multinodular goitre, thyroiditis, drug induced (iodine, Amiodarone) and toxic adenoma.
  3. Thyroid hormones control systemic metabolism, an excess will cause systemic defects
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2
Q 
Hyperthyroidism (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results - do Graves')
4. One differential
A
  1. Weight loss, irritability, heat intolerance, sweating, malaise, itching
  2. Tremor, hyperkinesis, exophthalmos, goitre
  3. Depends on aetiology (Graves’ Serum TSH is suppressed, serum fT3 and T4 elevated)
  4. Different causes of thyrotoxicosis
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3
Q 
Hyperthyroidism (red) 
Describe:
1. Management (1st line and adjuncts)
2. Complications
3. Prognosis
A
  1. Antithyroid drugs such as Carbimazole 20mg daily/methimazole - block hormone biosynthesis. Propanolol for symptom relief. May require surgery
  2. Thyroid crisis/storm - rapid deterioration of thyrotoxicosis triggered by stress (infection). Chronically - heart problems, brittle bones, eye problems, swollen skin
  3. Depends on aetiology, largely treatable.
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4
Q 
Graves' disease (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Autoimmune conditon of the thyroid causing hyperthyroidism
  2. The cause of this autoimmunity is not clear, liklely multifactorial
  3. TSH receptor antibodies stimulate the receptor cause excess thyroid hormones and the manifestation of disease.
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5
Q 
Graves' disease (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Anxiety, tremor or hands, weight loss, fatigue, heat insensitivity
  2. Goitre, thick red skin on top of shins (Graves’ dermopathy) and palpitations
  3. Serum TSH is suppressed (<0.5mlU/L). May test serum for autoantibodies
  4. Other causes of hyperthyroidism (toxic nodular goitre)
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6
Q 
Graves' disease (red) 
Describe:
1. Management (1st line and adjuncts)
2. Complications
3. Prognosis
A
  1. Antithyroid drugs (Methimazole) and propanolol for symptomatic relief
  2. Thyroid crisis, heart problems (AF, heart failure), brittle bones, eye problems
  3. With treatment excellent. Relapse is common and increased mortality if uncontrolled
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7
Q 
Hypothyroidism (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. A clinical state caused by the underproduction of thyroid hormones
  2. 95% are primary (Hashimotos being most common), 5% are secondary. Drugs that cause the condition are lithium, amiodarone etc.
  3. Thyroid hormones regulate metabolism and deficiency causes systemic effects
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8
Q 
Hypothyroidism (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. The diease is commonly asymptomatic, but if bad Weakness, lethargy, cold insensitivity, constipation, weight gain, depression, menstrual irregularity, myalgia
  2. Weight gain, slow speech, jaundice, bradycardia
  3. Serum TSH would be (often mildly) elevated. Can also detect antibodies
  4. Depression
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9
Q 
Hypothyroidism (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Levothyroxine (taken for life)
  2. Osteoporosis, AF, complications in pregnancy
  3. Excellent, usually full recovery when taking thyroid hormones
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10
Q 
Hashimotos thyroiditis (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Hypothyroidism due to aggressive autoimmune destruction of thyroid cells. Large number of antibodies and diffuse goitre
  2. Unknown, related to infections, smoking and iodine ingestion
  3. There is lymphocytic infiltration of T cells and autoantibodies. Some antibodies bind and block TSH receptors preventing secretion
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11
Q 
Hashimotos thyroiditis (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Those of hypothyroidism - fatigue, cold insensitivity, constipation, dry skin, muscle weakness, joint pain and stiffness, weight gain
  2. GOITRE
  3. Serum TSH is elevated with low fT3 and T4. May do antibody tests.s
  4. Other causes of hypothyroidism or depression
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12
Q 
Hashimotos thyroiditis (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Levothyroxine, taken for life. Resection of goitre
  2. Heart disease (due to high LDL), depression, myxoedma
  3. Excellent with treatment, worsens over years without treatment potentially causing organ damage.
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13
Q
  1. What are the 5 types of thyroid malignancy?

2. What is treament?

A
  1. Papillary, follicular, medullary, lymphoma, anaplastic

2. Surgical intervention

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14
Q 
Cushing's syndome (red) 
Describe:
1. Definition (the difference between disease and syndrome)
2. Aetiology
3. Pathophysiology
A
  1. Cushing’s disease is like a subset of Cushing’s syndrome. Both are excess corticosteroids , C disease is due to hyperfunction of the adrenal gland and Cushing’s syndrome excess corticosteroids due to a pituitary tumour producing too much ACTH
  2. Can also be caused from ectopic adenomas (lungs), or iatrogenic (steroids) most commonly)
  3. Disease is caused by excess cortisol (immune suppression, mobilising fuel (appetite) and bone breakdown)
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15
Q 
Cushings syndrome (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Weight gain, depression, lethargy, irritability, proximal weakness
  2. Central obesity (round face), skin and muscle atrophy (cortisol tries to get fuel for blood - appetite and catabolism) and purple striae (due to obesity). There may be Hyperpigmentation in C disease (raised ACTH)
  3. Overnight dexamethasone suppression test (give an exogenous steroid, should lower ACTH and endogenous steroids - measure morning cortisol - risen in Cushings)
  4. Alcoholism
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16
Q 
Cushings syndrome  (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. If iatrogenic, stop medication. If C disease pituitary adenectomy or resection of ectopic tumour. ACTH indepdent (C syndrome) do uni/bilateral adrenalectomy
  2. Increased risk of infection, weight gain, diabetes mellitus, osteoporosis
  3. Untreaed = high mortality usually from CVD. With normal cortisol levels seems to omprove normality
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17
Q 
Type 1 DM (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Raised blood sugar levels due to autoimmune destruction of beta cells
  2. Environmental antigens may cause the disease, or genetics
  3. 90% of patients have autoantibodies. Rapid loss of insulin causes hyperglycaemia. This stimulates glucagon secretion = hepatic glucose and ketogenesis.
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18
Q 
Type 1 DM (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Thirst, dry mouth, lack of energy, hunger, weight loss
  2. Polyuria, polydipsia, ketoacidosis
  3. Random glucose tolerance test, fasting plasma glucose
  4. T2DM/MODY
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19
Q 
Type 1 DM (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Insulin therapy (basal-bolus insulin)
  2. Microvascular = retinopathy, nephropathy, neuropathy. Macrovascular = CAD, cerebrovascular disease, PAD. Diabetic ketoacidosis
  3. Untreated is fatal due to diabetic ketoacidosis. Poorly controlled is RF for blindness, renal failure and amputations
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20
Q 
Type 2 DM (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. A progressive order defined be deficits in insulin secretion and action that lead to abnormal glucose metabolism
  2. Genetics has some part, mainly owed to RF like body weight, lack of exercise, smoking.
  3. There is progressive (10yrs) impaired insulin secretion and peripheral insulin resistance causing hyperglycaemia. The low insulin can prevent rapid weight loss and DKA
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21
Q 
Type 2 DM (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Same as T1DM (polyuria, polydipsia, blurred vision, weight loss, fatigue), but develop over years and in older patients
  2. Usually asymptomatic, can have risk factors such as UTIs and candida.
  3. Random glucose test >11.1mmol/L, Fasting plasma glucose
  4. T1DM
22
Q 
Type 2 DM (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. First-line Lifestyle changes, then Metformin and either SGTL-1i, DPP-IVi, GLP1 analogue, sulphonylurea
  2. Microvascular (retin, nephro, neuropathy), Macrovascular (CAD, PAD, cerebrovascular disease)
  3. Macrovascular events increase mortality, but risk depends on duration, glucose control and other factors
23
Q 
Conn's Syndome (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Adrenal glands make too much aldosterone (primary hyperaldosteronism)
  2. Not fully understood, genetic link, adrenal hyperplasia
  3. Aldosterone is released independent of its chronic regulator (RAAS). This causes excessive sodium (and water) reabsorption causing HTN. There is also hypokalaemia + metabolic acidosis if chronic.
24
Q 
Conn's Syndrome (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Often asymptomatic, or signs of hypokalaemia (weakness, cramps, paresthesia)
  2. HTN, low potassium, fatigue
  3. Blood tests U&E (serum potassium) would be low. Aldost/renin ratio high
  4. Essential HTN
25
Q 
Conn's Syndrome (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. If unilateral - Unilateral laparoscopic adrenalectomy. If bilateral - amiloride (thiazide diuretic that inhibits Na+ reabsorption (NCC symporter))
  2. Complications of HTN - cardiovascular events. Complications of hypokalaemia - AF, weakness, cramps
  3. Surgery cures, otherwise biochemical treatment cures patients.
26
Q

What causes secondary hyperaldosteronism?

A

This is excess aldosterone production due to high renin, often from decreased renal perfusion. Less common

27
Q 
Acromegaly (red) 
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. The abnormal growth of the hands, feet and face due to the overproduction of GH.
  2. Caused by a pituitary somatotroph adenoma in 95-99% of cases.
  3. This causes excessive GH and IGF-1 leading to the growth of hands, coersening of face, puffy lips, eyelids and skin
28
Q 
Acromegaly (red) 
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Acral (periphery) enlargement, Arthralgias (joint pain), Maxillofacial changes, excessive sweating, headache/backache, hypogonadal symptoms.
  2. Growth of hands, coarsening face, puffy lips, eyelids and skin, goitre
  3. Serum IGF-1, oral glucose tolerance test
  4. Pseudo-acromegaly
29
Q 
Acromegaly (red) 
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Transsphenoidal surgery. Dopamine agonists/somatostatin antagonists can suppress GH as adjunct
  2. Higher mortality from cardiac complucations (LVH), HTN, osteoarticular complications, diabetes, carpal tunnel
  3. Increased mortality, bit getting better
30
Q 
SIADH (orange)
Describe:
1. Definition
2. Aetiology
3. Pathophysiology (describe serum Na+, osmolality and urine Na+, osmolality)
A
  1. Euvolemic, hypotonic hyponatraemia secondary to impaired free water secretion, usually from excessive ADH.
  2. Increased ADH secretion/responsiveness can be caused by drugs (Amiodarone), ectopic ADH source (lung), brain injury, genetic V2 receptor defects
  3. Due to increased ADH and WATER reabsorption there is:
    Decreased plasma Na+ and osmolality and increased urine Na+ and osmolality
31
Q 
SIADH (orange)
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Depends on the rate of development and severity of hyponatraemia. Mild - asymptomatic, moderate - nausea, vomiting, headache, confusion, weakness. Severe - seizures and comas
  2. Urine concentrated and blood dilute. No signs of hypovolaemia (tachycardia)
  3. Serum sodium (low<130mmol/L) and serum osmolality. May test urine
  4. Hypovolaemia
32
Q 
SIADH (orange)
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Acute (asyomptomatic) = fluid restriction (+ IV hypertonic saline if symptomatic)
  2. Central pontine myelinolysis, cerebral oedema, seizures and coma
  3. If not treated, very serious. Condition resides once underlying condition is treated
33
Q

Name the three types of hyponatraemia, a cause and their treatment.

A
  1. Fluid overload (dilutional), inappropriate IV - restrict fluid
  2. Normovolaemic, SIADH - restrict fluid
  3. Dehydrated (hypovolaemic), vomiting, diuretics - hypertonic saline + restrict fluid
34
Q 
Hypokalaemia (orange)
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Serum potassium <3.5mmol/L (<2.5 is severe)
  2. Caused by increase K+ into cells, renal excretion (Conn’s/PA), extrarenal losses
  3. Potassium determines membrane potential, so can have neuromsuclar effects
35
Q 
Hypokalaemia (orange)
Describe:
1. Symptoms/Signs
2. Main investigations (and their results)
3. One differential
A
  1. Acute - muscle weakness, ECG changes. Chronic - rhabdomyolysis, renal abnormalities
  2. ECG, serum potassium
  3. Alcoholism
36
Q 
Hypokalaemia (orange)
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Treat underlying cause (e.g. assess diuretics). Potassium replacement is given in severe/symptomatic patients. Monitor to avoid HyperK
  2. Severe muscle weakness/paralysis, AF, renal dysfunction
  3. Can cause death, but prognosis depends on condition
37
Q 
Hyperkalaemia (orange)
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Serum potassium >5.0mmol/L. Differentiate from artefactual hyperkalaemia
  2. Usually caused by impaired potassium excretion (Addison’s disease (hypoaldos), kidney injury, drugs (NSAIDs)) or increase extraneous load
  3. Potassium control cellular membrane potentials which are disrupted.
38
Q

Hyperkalaemia (orange)
Describe:
1. Symptoms/Signs
2. Main investigations (and their results)

A
  1. Usually few signs/symptoms until levels are high enough to cause cardiac arrest. May produce impaired neuromuscular transmission (weakness, paralysis) and respiratory compensation
  2. ECG and serum potassium
39
Q 
Hyperkalaemia (orange)
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Mild to moderate is managed by diet potassium restriction. Severe is a medical emergency - give insulin to drive K+ into cells, give calcium gluconate
  2. Cardiac arrhythmias, muscle weakness, paralysis
  3. If untreated, threatness life and end organ damage
40
Q 
Diabetes Insipidus (orange)
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Rare disorder when ADH is deficiency or ineffective.
  2. Can be caused by nephrogenic DI (resistance to ADH) or Cranial DI (no ADH released)
  3. A lack of ADH causes poor water reabsorption and urine concentrating leading to patient being constantly thirsty (concentrated serum) with inappropriately dilute urine. The patient must be normo/hypernatraemic
41
Q 
Diabetes Insipidus (orange)
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Constantly feeling thirsty, polydipsia, polyuria
  2. Urine osmolality <200 (dilute) AND serum osmolality >300 (normal is 285-295, high).
  3. Hypertonic saline infusion and measure AVP/copeptin. ADH would not rise in DI
  4. Diabetes mellitus
42
Q 
Diabetes Insipidus (orange)
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. CDI - treat underlying condition and give ADH analogue (Desmopressin). NDI is difficult to treat, make sure they have water access
  2. Bladder dysfunction and renal impairment. Short term - hypernatraemia, thrombosis
  3. CDI and NDI can resolve with treatment but require lifelong follow ups.
43
Q

What are the 2 opposites to Addison’s disease (primary adrenal insufficiency)?

A

Conn’s disease (primary hyperaldosteronism)

Cushing’s syndrome/disease (hypercortisolism)

44
Q 
Addison's disease (orange)
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Autoimmune destruction of the entire adrenal cortex by organ specific antibodies. It is rare.
  2. Caused by immune dysfunction, often triggered by TB, viruses and bacteria
  3. Decreased levels of aldosterone, cortisol and DHEA cause disease. Mainly, we are worried about a decrease in cortisol, the stress hormone which increases glucose metabolism, maintains circulation and suppresses immune system
45
Q 
Addison's disease (orange)
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Fatigue, anorexia, weight loss, dizzyness, poor recovery from illness
  2. PIGMENTATION due to raised ACTH, low blood pressure
  3. Short ACTH stimulation (Give ACTH, if cortisol remains low the +), monring serum cortisol
  4. Adrenal suppression due to corticosteroid therapy. Secondary AI
46
Q 
Addison's disease (orange)
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Hydrocortisone (pharmaceutical cortisol) + mineralocorticoid. Depends on patient
  2. Adrenal crisis, low blood pressure, depression, hypoglycaemia
  3. If patients forget treatment it can be fatal (crisis), and require treatment for life - but well treated.
47
Q

Describe adrenal crisis

  1. Cause
  2. Signs/symptoms
  3. Treatment
A
  1. If Addisons is left untreated, levels of hormones drop to life-threatening levels. If we encounter stress (no cortisol) symptoms appear quickly and severely.
  2. Cardiovascular collapse, fatigue, fever, vomiting, weakness, confusion, collapse
  3. Give hydrocortisone IV without a doubt to prevent death
48
Q 
Secondary adrenal insufficiency (orange)
Describe:
1. Definition
2. Aetiology
3. Pathophysiology
A
  1. Like addison’s disease (underfunctioning of adrenals) but due to reduced pituitary or hypothalamic activity = too little ACTH
  2. Caused by pituitary tumours, trauma of hypothalamus/pituitary. Can very commonly be caused by exogenous steroids inhibiting ACTH production
  3. Too little ACTH causes too little arenal cortex hormones
49
Q 
Secondary adrenal insufficiency (orange)
Describe:
1. Symptoms
2. Signs
3. Main investigations (and their results)
4. One differential
A
  1. Same as Addisons - fatigue, weight loss, dizzyness, faints, poor recovery from millness, adrenal crisis
  2. Same as Addisons but NO PIGMENTATION (low blood pressure)
  3. Serum a.m. cortisol, ACTH stimulation test
  4. Addison’s disease
50
Q 
Secondary adrenal insufficiency (orange)
Describe:
1. Management (1st line)
2. Complications
3. Prognosis
A
  1. Treat adrenal crisis, give hydrocortisone. Surgery may be indicated for tumours
  2. Adrenal crisis, low blood pressure, depression
  3. If treated (surgery, stop steroids), usually resolves

Jack Misc List (9 decks)

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