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Phase 2a flashcards (Alec's) > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Give a simple definition of type 1 diabetes

A

Autoimmune destruction of the pancreatic beta cells –> complete insulin deficiency

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2
Q

What type of hypersensitivity reaction is T1DM?

A

4

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3
Q

What are 3 risk factors for T1DM

A

Northern European
Other autoimmune diseases e.g. coeliac, rheumatoid arthritis
Gene mutations/ variants

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4
Q

Which specific genes may be different in T1DM and where are they found (what cell)

A

HLA DR3-DQ2
HLA DR4-DQ8

Found on Beta cells (they express HLA genes)

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5
Q

Epidemiology of T1DM (3 things)

A

Age usually 5-15
BMI < 25
10% of all diabetes

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6
Q

How does T1DM cause hyperglycaemia?

A

B cells attacked –> insulin deficiency –> gluconeogenesis, glycogenlysis, decreased cell uptake of glucose

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7
Q

How does T1DM cause hyperkalemia (in blood)?

A

Insulin stimulates Na+/K+ ATPase pumps, therefore lack of insulin means K+ can’t get in cells

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8
Q

How is T1DM diagnosed?

A

RPA > 11.1 mmol/l
FPG > 7 mol/l
HbA1C >48 mol/l or 6.5%

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9
Q

Signs/ symptoms of T1DM (3)

A

Polydipsia
Polyuria
Weight loss (can’t get glucose in cells)

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10
Q

Treatment of T1DM

A

SC fat insulin injection

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11
Q

Rapid acting insulin name

A

aspart

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12
Q

Short acting insulin name

A

regular insulin

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13
Q

Intermediate acting insulin name

A

NPH (Neutral protamine hagedorn)

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14
Q

Long acting insulin name

A

Glargine

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15
Q

What is DKA (simple)

A

Complication of diabetes (usually type 1) where lack of insulin = high ketone levels, acidosis and hyperglycaemia

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16
Q

Pathology of DKA (hyperglycaemia, acidosis and high ketone levels)

A

No insulin –> hyperglycaemia (but cells starved of glucose) –> lipolysis/ ketogenesis –> increase in ketones in blood –> acidosis (initially buffered by bicarbonate)

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17
Q

What might bring on DKA

A

Illness/ infection

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18
Q

Symptoms of DKA (4)

A

Diabetes symptoms
Nausea/ vomiting
Confusion/ drowsiness
Abdo pain (liver stretches)

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19
Q

Signs of DKA (4)

A

Kussmaul breathing (deep+fast to expel CO2)
Pear drop breath
Hypotension (hypovolaemic)
Tachycardia

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20
Q

Diagnosis of DKA

A

RPG > 11 mmol/l
Plasma ketones > 3 mmol/l
Blood pH < 7.35 or Bicarb < 15 mmol/l

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21
Q

Treatment of DKA

A
  1. ABC (emergency)
  2. Fluids (0.9% saline)
  3. IV regular insulin and K+
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22
Q

Why is K+ essential to treat DKA with

A

Insulin makes K+ enter cells therefore K+ will immediately enter cells when insulin administered, so K+ in the blood must be restored to prevent cardiac arrest

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23
Q

Complications of DKA (3)

A

Coma/ death
Cerebral oedema
Aspiration pneumonia

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24
Q

What is T2DM (simple)

A

Peripheral insulin resistance and may lead to insulin deficiency

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25
Q

Pathology of T2DM

A

Repeated insulin exposure –> insulin resistance –> more insulin required for response –> beta cells grow tired + stop working –> insulin deficiency

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26
Q

T2DM risk factors (6)

A

Age (30+)
Male
Obesity
Sedentary
African or South Asian
Genetics

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27
Q

Signs + symptoms of T2DM (7)

A

Fatigue
Polydipsia + polyuria
Glucosuria
Slower onset > 6 months
Central obesity
Slow healing + infections (bad circulation)
Blurred vision (once progressed)

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28
Q

Diagnoses of T2DM (4 ways) and diagnostic values

A

Fasting plasma glucose = after 8 hours
Oral glucose tolerance test = 75g glucose drink after fast then measure glucose level 2 hours later

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29
Q

What are the 5 steps to manage T2DM

A
  1. Lifestyle changes
  2. Metformin
  3. Double therapy
  4. Triple therapy
  5. Insulin
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30
Q

What class of drug is metformin

A

Biguanide

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31
Q

How does Metformin work (2)

A
  • Decrease liver gluconeogenesis
  • Increase cell sensitivity to insulin
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32
Q

Metformin side effects (2)

A
  • GI disturbances
  • lactic acidosis, as no gluconeogenesis. (can be serious)
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33
Q

What can metformin be used in combination with (4)

A
  • DPP 4 inhibitors
  • Sulfonylurea - cause Beta cells to make more insulin (glicazide)
  • Pioglitazone - improve insulin sensitivity
  • SGLT-2 inhibitors
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34
Q

What is hyperosmolar hyperglycaemic state (simple)

A

Hyperglycaemia without ketosis

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35
Q

What is the pathophysiology of HHS how does it cause hyperglycaemia and dehydration?

A

Low insulin –> hyperglycaemia
(Insulin not absent therefore ketogenesis does not occur)

Hyperglycaemia –> glucose sucks water out of blood –> dehydration

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36
Q

What may bring on HHS in those with diabetes?

A

Infection/illness

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37
Q

Signs/ symptoms of HHS (4)

A
  • Diabetes symptoms
  • Confusion
  • Dehydration
  • Lethargy
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38
Q

Investigations for HHS (4)

A
  • RPG = high
  • Urine dipstick = glycosuria
  • Plasma osmolality > 320 mOsm/kg
  • No ketones in urine
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39
Q

Treatment for HHS

A
  1. Fluid replacement (0.9% saline)
  2. Insulin - slow infusion; with K+
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40
Q

What is diabetes insipidus (simple)

A

A lack of ADH or a lack of response to ADH

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41
Q

What are the 2 types of DI

A
  • Nephrogenic - collecting ducts don’t respond to ADH
  • Cranial - impaired production/ secretion from hypothalamus/ post. pituitary
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42
Q

Where does ADH take effect and what channel does it effect?

A
  • V2 receptor - increases expresion of AQ2 in collecting ducts of kidneys; increases reabsorption of Na+ in the collecting ducts.
  • V1 receptor - causes vasoconstriction
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43
Q

Where is AQ1 found

A

Proximal convoluted tubules and descending limb of LoH

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44
Q

What is primary polydipsia

A

Some idiot drinking too much

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45
Q

What causes nephrogenic DI (4)

A
  • Drugs (e.g. lithium for BPD)
  • Renal disease
  • Electrolyte imbalances (damage nephrons)
  • Congential/ inherited/ mutation
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46
Q

What causes cranial DI (5)

A
  • Idiopathic
  • Brain tumours
  • Head injury
  • Congential/ mutation
  • Infection (meningitis)
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47
Q

Signs/ symptoms of DI (4)

A
  • polyuria/ polydipsia
  • dehydration
  • Postural hypotension
  • Hypernatraemia (hypovolemic)
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48
Q

How much urine is suspicious of DI

A

3 litres in 24 hours

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49
Q

What is the diagnostic test for DI and describe it

A

Water deprivation test:
* no fluids 8 hours - measure urine osmolality
* give synth. ADH - measuere urine osmolality 8 hours later

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50
Q

What are the expected results of water deprevation test for cranial DI, nephrogenic DI and pimary polydipsia

A
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51
Q

What other investigations may be done for DI (3)

A
  • Urine dip
  • U&Es
  • Cranial MRI (check for tumours…)
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52
Q

Compliactions of DI (2)

A
  • Dehydration
  • Electrolyte imbalance
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53
Q

Treatment for DI

A

Treat underlying cause
* rehydration for mild
* Cranial - desmopressin
* Nephrogenic - thiazide diuretic: bendroflumethiozide

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54
Q

How do thiazide diuretics work

A

Block Na-Cl co-transporters and blarrrrr blarrrrr blarrrrrrrrr
But nobody has a fucking clue

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55
Q

What is syndrome of inappropriate ADH (simple)

A

Large amounts of ADH cause excess fluid to be reabsorbed in collecting duct

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56
Q

Pathophysiology of SIADH - how does it cause excess reabsorption of water

A

Excess ADH is produced/ secreted–> increase expression of AQ2 in collecting duct –> increased reabsorption of water

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57
Q

Why does euvolaemic hyponatraemia occur in SIADH

A

Sodium is excreted from kidneys to compensate for the over reabsorption of water. As water follows sodium the correct fluid volume is maintained, however the body is low in sodium.

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58
Q

What causes SIADH (4)

A
  • Infection
  • Head injury
  • Medications
  • Tumours (secrete ADH)
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59
Q

Which tumours can secrete ADH (5)

A
  • SCLC
  • Prostate
  • Thymus
  • Pancreatic
  • Lymphomas
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60
Q

Which medications cause SIADH (3)

A
  • Thiazide diuretics
  • NSAIDs
  • SSRIs
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61
Q

What are the symptoms of SIADH (4), (signs in next card)

A
  • N+V
  • Headache
  • Fatigue
  • confusion

siezures + reduced consiousness more severe symptoms of hyponatraemia

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62
Q

What are the signs of SIADH (3)

A
  • Raised jugular vein pressure
  • Oedema
  • Ascites
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63
Q

How is SIADH diagnosed

A

It is a diagnosis of exclusion
* U&E –> hyponatraemia and normal K
* Urine sodium + osmolality = high

Exclude other causes of hyponatraemia e.g. CKD, diuretic use…

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64
Q

How is SIADH managed (what medicine is used)

A
  1. Treat cause
  2. Fluid restriction
  3. Tolvaptan - ADH receptor antagonist; Furosemide - strong diuretic
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65
Q

What are some complications of SIADH (4)

A
  • Cerebral oedema
  • Siezures
  • Coma
  • Central pontine myelinolysis
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66
Q

How does SIADH cause central pontine demyelinolysis

A

Na+ low in blood –> solutes move out of brain to prevent cerebral oedema
Hyponatraemia treated too quickly
Blood Na+ rises quickly –> water moves out of brain quickly –> demyelination of neuones

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67
Q

What is Cushing’s syndrome (simple)

A

Chromic excess of cortisol

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68
Q

Where is cortisol released from

A

zona fasiculata of the adrenal gland

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69
Q

Describe the HPA axis

A

Hypothalamus releases corticotropin releasing hormone –> anterior pituitary releases adrenocorticotropin releasing hormone –> adrenal gland releases cortisol

This is regulated by negative feedback

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70
Q

Cortisol actions in body (5)

A
  • Inhibits immune system
  • Increases blood glucose
  • Increases alertness
  • Increases metabolism
  • Inhibits bone formation

All more long term flight/ fight responces

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71
Q

Causes of cushing’s ACTH dependant (2)

A
  • Cushings disease - pituitary adenoma releases ACTH –> adrenal hyperplasia
  • Ectopic ACTH - from SCLC
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72
Q

Causes of Cushing’s ACTH independant (2)

A
  • Adrenal adenoma - secretes cortisol
  • Iatrogenic steroid use (corticosteroids)

iatrogenic = caused by medical procedure or treatment

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73
Q

What are the sign and symptoms of Cushing’s (5)

A
  • Moon face (round)
  • Central obesity
  • Buffalo hump (fat on shoulders)
  • Abdominal striae
  • Osteoporosis
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74
Q

How is Cushing’s syndrome investigated

A
  • Random plasma cortisol levels, if abnormal…
  • Dexamethasone suppression test, if abnormal…
  • Plasma ACTH
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75
Q

How is random plasma cortisol levels different in those with cushing’s

A

Does not follow typical diurnal pattern (high in morning, low at night)
And generally higher overall

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76
Q

What is dexamethasone

A

Binds to same receptors as cortisol (therefore inhibits ACTH)

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77
Q

Describe how the low dose dexamethasone supression test works

A

1 mg DM given @10pm –> cortisol measured @9am
Low cortisol = normal
High/ normal cortisol = cushing’s

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78
Q

Describe how the high dose dexamethasone supression test works

A

8mg DM given @10pm –> ACTH and cortisol measued @9am
Low cortisol = cushings disease (-ve feedback in high dose able to suppress pit adenoma)
High/ normal cortisol and low ACTH = adrenal adenoma
High/ normal cortisol and high ACTH = ectopic ACTH tumour

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79
Q

How is Cushing’s treated (2)

A
  • Treat/ stop underlying cause (excise tumour/ stop meds)
  • Remove adrenal glands and give steroidal treatment
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80
Q

What are some compliactions of cushing’s (3)

A
  • Diabetes (cortisol increases blood glucose so cells can become resistant to insulin)
  • Hypertension/ CVD
  • Osteoporosis
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81
Q

What is adrenal insufficiency (simple)

A

Adrenal glands dont produce enough steroid hormones (cortisol and aldosterone)

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82
Q

What are the two types of adrenal insufficiency

A
  • Primary AI (Addison’s disease) = adrenal cortex damaged
  • Secondary AI = pituitary/ hypothalamic involvement (low ACTH/ CRH)
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83
Q

Pathophysiology of two types of adrenal insufficiency

A

Primary - adrenal gland damaged = low steroids –> hight ACTH to try to compensate
Secondary - low CRH/ACTH –> low steroidal hormones

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84
Q

What are some causes of Addison’s disease (2)

A
  • Autoimmune destruction - 80% of cases in UK
  • TB infection - damages adrenal gland
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85
Q

What antibody is often present in those with Addison’s

A

21-hydroxylase antibody

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86
Q

What causes secondary AI (5)

A
  • Surgery
  • Infection e.g. meningitis
  • Radiotherapy
  • Necrosis
  • Iatrogenic - supression of HPA
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87
Q

What are some symptoms of AI (5)

A
  • Fatigue/ weakness
  • Weight loss
  • Nausea
  • Decreased libido
  • Change in body hair

(Dermatological stuff in the signs card)

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88
Q

What are some signs of AI

A
  • Dermatological - hyperpigmentation and vitiligo
  • Hypoglycaemia
  • Postural hypotension
89
Q

What causes hyperpigmentation in AI and therefore which type is affected

A

ACTH stimulates melanocytes to produce melanin
Therefore occurs in primary AI as lots of ACTH produced to compensate for damaged adrenal gland

90
Q

What is a severe presentation of AI known as and what are the symptoms/ signs (3)

A

Addisonian/adrenal crisis
* reduced consciousness
* hypotension
* low NA+, hypoglycaemia, high K+

91
Q

How is adrenal insufficiency investigated (2)

A

1st line: U&Es –> low sodium, high potassium, hypoglycaemia
Gold: short syncathen test

21-hydroxylase autoABs test

92
Q

How does the short syncathen test work

A

Syncathen (synthetic ACTH) is administered –> cortisol levels monitored @baseline, 30 min and 60min –> if cortisol doesn’t increase by much (doesn’t double) = Addisons

93
Q

How can secondary AI be diagnosed

A

Cortrosyn (synthetic CRH) administered –> affect an ACTH monitored

94
Q

How is AI treated (name sof meds)

A
  • Hydrocortisone (glucocorticoid) - to replace cortisol
  • Fludrocortisone (mineralcorticoid) - to replace aldosterone
95
Q

What should you do to AI medication during illness/ trauma

A

Double the dose to mimic stress responce

96
Q

What is phaeochromocytoma (simple)

A

Tumour of the chromaffin cells of the adrenal medulla that secrete catecholamines

97
Q

What pattern is adrenaline usually secreted in (for people with phaeochromocytoma)

A

Secreted in bursts, so periods of worse symptoms followed by settled periods

98
Q

Which hormones are catecholamines (3)

A
  • Adrenaline
  • Noradrenaline
  • Dopamine
99
Q

What condition are phaeochromocytoma associated with

A

Multiple endocrine neoplasia type 2 (MEN type 2)

100
Q

What is the pattern of phaeochromocytoma tumours (4 things)

A
  • 10% bilateral
  • 10% outside adrenal glands
  • 10% cancerous
  • 25% familial
101
Q

What are the symptoms of phaeochromocytoma (think adrenaline) (4)

A
  • Headache
  • Sweating
  • Cardiac - palpitations, tachycardia
  • Tremor
102
Q

What are some signs of phaeochromocytoma (2)

A
  • Hypertension (hypertensive retinopathy)
  • Pallor (looking pale)
103
Q

How are phaeochromocytoma investigated

A
  • Plasma metanephrines/ normetanephrines
  • 24 hour urine catecholamines
  • CT - look for tumour
104
Q

What are metanephrines and why are they measured

A

Metabolites of adrenaline
They have a longer half life so less prone to fluctuation

105
Q

How is phaeochromocytoma treated

A
  • Medication (alpha/ beta blockers)
  • Adrenalectomy = definitive treatment
106
Q

What medication is used to treat phaeochromocytoma

A
  • Alpha blocker - blocks noradrenaline
  • Beta blocker - blocks adrenaline (prevents reactive vasoconstriction)
107
Q

What is an example of an alpha blocker used in phaeochromocytoma?

A

Phenoxybenzamine

108
Q

What is an example of a beta blocker

A

Atenolol

109
Q

How is a hypertensive crisis treated in pheochromocytoma?

A

Phentolamine (antihypertensive alpha blocker)

110
Q

What defines a hypertensive crisis

A

120/180

111
Q

What is primary hyperaldosteronism (simple)

A

Overproduction of aldosterone idependant of the RAAS system

112
Q

What causes primary hyperaldosteronism (2)

A
  • Adrenal adenoma (Conn’s syndrome)
  • Bilateral adrenal hyperplasia
113
Q

What is the pathophysiology of primary hyperaldosteronism (how are electrolytes affected)

A

More aldosterone produced –> high NA+ reabsorption, high H2O reabsorption, high K+ excretion

114
Q

What are the signs/ symptoms of Conn’s (4)

A
  • Hypertension
  • Electrolyte disturbance - arrhythmias, cramps, mood changes…
  • Fatigue
  • Polyuria/dipsia - low K+ interferes with kidney function
115
Q

How is primary hyperaldosteronism investigated

A
  • Low plasma K+
  • Aldosterone high, renin low blood test
116
Q

How is primary hyperaldosteronism treated

A
  • Adrenalectomy for adenomas
  • Aldosterone antagonist for bilateral hyperplasia
117
Q

What is an example of an aldosterone antagonist

A

Spironolactone

118
Q

What is secondary hyperaldosteronism

A

High rennin –> high aldosterone
(Not ACTH because this is Cushing’s disease)

119
Q

What usually causes secondary hyperaldosteronism

A

Disproportionatly low renal BP
(low renal BP)

120
Q

What is hyperthyroidism (simple)

A

Excess thyroid hormones

121
Q

What is the pathophysiology of hyperthyroidism (2 types)

A
  • Primary - thyroid produces excess T3/4 independant of TSH
  • Secondary - thyroid produces excess T3/4 due to overstimulation by TSH
122
Q

Which thyroid hormone is active

A

T3 = triiodothyronine

123
Q

What are the effects of T3 (4)

A
  • Increase metabolism
  • Activates SNS
  • Increases bone resporption
  • Increases cardiac output
124
Q

Who is mainly affected by hyperthyroidism

A

Women, 20-40 yrs

125
Q

What is the prevelance of Grave’s disease in the population

A

0.5%

126
Q

What causes primary hyperthyroidism (4)

A
  • Grave’s disease - TSH receptor autoantibodies mimic TSH and stimulate thyroid gland
  • Toxic multinuclear goitre - nodules on thyroid produce thyroid hormone independant of feedback
  • Thyroid cancer
  • Thyroiditis e.g. De Quervains - first hyperthyroidism then hypo due to negative feedback then return to normal
127
Q

What causes secondary hyperthyroidism (2)

A
  • Pituitary adenoma
  • Hypothalamic pathology
128
Q

What are some risk factors for graves disease?(2)

A
  • Family history (gene HLA-DR3)
  • Other autoimmune conditions

These are only really for Graves disease

129
Q

What are some symptoms of hyperthyroidism (4)

A
  • Hot and sweaty
  • Weight loss + hyperphagia (being hungary)
  • Irritable/ anxious
  • Diarrhoea
130
Q

What are some signs of hyperthyroidism (general - 2)

A
  • Tachycardia
  • Muscle waisting
131
Q

How is hyperthyroidism investigated

A
  • T4 and TSH plasma levels
  • TSH-R auto ABs
  • US and UT thyroid/ pit
132
Q

How would T4 and TSH be affected in hyperthyroidism, primary and secondary

A
  • Primary = T4 high, TSH low
  • Secondary = T4 high, TSH high
133
Q

How is hyperthyroidism managed (4)

A
  • Adrenergic receptor blockers - e.g. beta blockers, propranolol (non selective)
  • Medicines to block thyroid uptake of iodine
  • Radioactive iodine - kills thyroid cells, (patient must stay away from kids for few days)
  • Surgery

Levothyroxine if patient becomes hypo

Adrenergic receptor blockers used to treat syptoms as T3 activates SNS

134
Q

What are two medications used for hyperthyroidism

A
  • Carbimazole = 1st line
  • Propylthiouracil = 2nd line
135
Q

What are some complications of hyperthyroidism (not gaves complications) (2)

A
  • Thyroid storm = emergency - very high T3/4 levels; fever, high HR
  • Osteoporosis
136
Q

How is thyroid storm treated

A

Same way as hyperthyroidism + supportive treatment e.g. Carbimazole, beta blockers

137
Q

What antibody class causes Grave’s disease

A

IgG

138
Q

What is the pathophysiology of Graves

A

Auto ABs stimulate TSH-R and mimick TSH.
They also affect other body parts such as muscles behind the eyes causing inflammation.

139
Q

What are the symptom unique to Grave’s (3)

A
  • Goitre (swollen thyroid)
  • Exophthalmos - bulging eyes
  • Pretibial myxoedema - buildup of mucin under skin on anterior part of leg
140
Q

What is hypothyroidism (simple)

A

Lack of thyroid hormones - T3/4

141
Q

What are the two types of hypothyroidism

A
  • Primary - thyroid pathology = less T3/4 independant of TSH
  • Secondary - ant. pituitary/ hypothalamic pathology = too little TSH produced/ released sometimes called hypopituitarism
142
Q

Who does hypothyroidism mainly affect (2 things)

A
  • Over 40s
  • Females (6:1)
143
Q

What causes hypothyroidism (5)

A
  • Hasimoto’s thyroiditis
  • Iodine deficiency
  • Drugs - hyperthyroid drugs, lithium
  • Thyroidectomy
  • Hypopituitarism - infection, tumour, radiation
144
Q

What is the pathophysiology of Hashimoto’s thyroid

A

AutoABs (e.g. antithyroid peroxidase) attack thyroid gland –> swelling (goitre) –> then atrophy of thyroid

145
Q

What are some risk factors of hypothyroidism

A

Other AI diseases

146
Q

What are some symptoms of hypothyroidism (5)

A
  • Weight gain
  • Fatigue/ lethargy
  • Constipation
  • Cold intolerance
  • Menorrhagia (heavy periods)
147
Q

What are some signs of hypothyroidism (4)

A
  • Bradycardia
  • Delayed reflexes
  • Goitre
  • Oedema
148
Q

How is hypothyroidism investigated and what would the results be

A

Thyroid function tests
* Primary = low T3/4, high TSH
* Secondary = low T3/4, low TSH

149
Q

How is hypothyroidism treated

A

Adress underlying cause
then… levothyroxine

150
Q

What is levothyroxine and what happens to it in body

A

T4 - metabolised to T3

151
Q

What are some complications of hypothyroidism (3)

A
  • Congestive cardiac failure
  • Myxoedema coma (hypothermia, difficulty breathing, confusion)
  • Pregnancy problems
152
Q

What is hyperparathyroidism

A

Too high levels of PTH in the blood

153
Q

What are the effects of PTH on Ca2+ (3 things)

A
  • Increase reabsorption of Ca2+ in kidneys
  • Increase reabsorption of bone (more osteoclast activity)
  • Activate vitamin D3 in kidneys
154
Q

What effects does Vitamin D3 have on Ca2+ (4 things)

A
  • Ca2+ absorption in intestines
  • Ca2+ reabsorption in kidneys
  • Ca2+ resorption from bone
  • Negative feedback on PTH
155
Q

What effect does PTH have on phosphate

A
  • Decreases reabsorption of phosphate in kidneys
    Overall small decrease in phosphate serum levels
156
Q

Why does a decrease in phosphate mean an increase in Ca2+

A

Phosphate forms salts with Ca2+, therefore a decrease in phosphate = more ionised calcium circulating

157
Q

Which cells produce PTH

A

Chief cells in the parathyroid gland

158
Q

What are the three types of hyperparathyroidism

A
  • Primary = Excessive inapropriate production of PTH
  • Secondary = hypocalcaemia –> high PTH to compensate
  • Tertiary = autonomous production of PTH after resolution of hypocalcaemia due to hyperplasia
159
Q

Main cause of primary hyperparathyroidism

A

Parathyroid adenoma

160
Q

Causes of secondary hyperparathyroidism (2)

A
  • CKD –> low reabsorption of Ca2+
  • Low vit D intake –> decreased absorption of Ca2+ from intestines
161
Q

Cause of tertiary hyperparathyroidism

A

Prolonged secondary –> hyperplasia of PT gland; unresponsive to -ve feedback

162
Q

What are the signs/ symptoms of hyperparathyroidism (5)

A
  • Renal stones
  • Painful bones
  • Abdominal groans - constipation, N+V
  • Psychiatric moans - fatigue/ depression
  • Polyuria/dipsia = going to toilet more - thrones
163
Q

How is hyperparathyroidism investigated

A
  • PTH/ Ca2+/ phosphate blood tests
  • DEXA scan
164
Q

What would PTH, Ca and phosphate be in primary, secondary and tertiary hyperparathyroidism

A
165
Q

How is hyperparathyroidism managed

A
  • Primary - parathyroidectomy; medication to slow bone loss
  • Secondary - calcium correction
  • Tertiary - medication to increase calcium sensitivity; parathyroidectomy
166
Q

What medicine is used to slow bone loss in primary hyperparathyroidism

A

Bisphosphonates

167
Q

What medicine is used to increase calcium sensitivity of the parathyroid gland in hyperparathyroidism

A

Cinacalcet

168
Q

What is hypoparathyroidism

A

A lack of plasma PTH

169
Q

What are the types of true hypoparathyroidism

A
  • Primary - pt glands dont produce enough PTH for whatever reason
  • Secondary - pt glands dont produce enough PTH due to hypercalcaemia
170
Q

What causes primary hypercalcaemia (3)

A
  • Surgery/ damage/ radiation
  • Genetic malformations
  • Auoimmune
171
Q

What are the symptoms of hypoparathyroidism (4)

A
  • Convulsions
  • Arrhythmias
  • Tetany
  • Numbness

CATs go NUMB

172
Q

What are the signs of hypoparathyroidism (2)

A
  • Trosseau’s sign - flexion of wrist when BP cuff put on
  • Chvostek’s sign - spasm of facial muscles when CN7 tapped over parotid gland

These signs are due to increased firing of nerves due to hypocalcaemia

173
Q

How is hypocalcaemia diagnosed (2)

A
  • PTH low, Ca2+ low, phosphate high
  • ECG = long QT syndrome
174
Q

How is hypocalcaemia treated

A

Treat underlying cause
Give Ad Cal D3 (calcium and vitamin D3 to increase Ca2+ absorption)

175
Q

What is pseudohypoparathyroidism

A

Lack of responce to PTH at bones and kidneys and can’t activate calcidiol

176
Q

What is acromegaly (simple)

A

Excessive release of GH –> overgrowth of systems

177
Q

What stimulates GH release

A

Growth hormone releasing hormone

178
Q

What else stimulates GH release

A

Ghrelin

179
Q

What hormones inhibit growth hormone release (2)

A
  • Somatostatin - major effect
  • Dopamine - minor effect
180
Q

What does GH stimulate the release of that also exerts affects throught the body

A

Insulin like growth factor-1

181
Q

Where is ILGF-1 released from

A

Liver

182
Q

What are the effects of GH and ILGF-1 (5)

A
  • Increase muscle growth
  • Increase bone density
  • Increase protein synthesis
  • Increase fat/ glycogen breakdown
  • Inrcease cell reproduction
183
Q

What causes acromegaly

A
  • Pituitary adenoma
  • Lung/ pancreatic GHRH or GH secreting tumour
184
Q

What are the signs/ symptoms of acromegaly (5)

A
  • Changes in body shape/ features
  • Bitemporal hemianopia
  • Arthritis - growth of joint tissues
  • Sleep aponea
  • Fatigue
185
Q

What changes in body shape/ features occur in acromegaly

A
  • Large hands/ feet
  • Prominent forehead
  • Mandibular protrusion
186
Q

What does acromegaly in children cause

A

Gigantisism

187
Q

How is acromegaly investigated

A
  • ILGF-1 blood test = raised
  • OGTT while measuring GH
188
Q

Why is ILGF-1 measured instead of GH for acromegaly diagnosis

A

ILGF-1 doesn’t fluctuate like GH does throught the day

189
Q

How is OGTT used to diagnose acromegaly

A

Glucose drink given –> GH monitored, should be surpressed by high glucose levels

190
Q

How is acromegaly managed

A
  • Transphenoidal resection surgery
  • Medication to inhibit GH
191
Q

What medication is used to treat acromegaly (3)

A
  • Somatostatin analogue (ocreotide)
  • Dopamine agonist (bromocriptine)
  • GH receptor antagonists (pegvisomant)
192
Q

What are some complications of acromegaly

A
  • T2DM
  • Sleep apnoea
  • IHD
  • Colorectal cancer
193
Q

What is a prolactinoma

A

Pituitary adenoma that secretes excess prolactin

194
Q

What are the two types of prolactinoma tumours

A
  • micro - less than 10mm on mri
  • macro more than 10mm on mri
195
Q

What are the functions of prolactin (2)

A
  • Stimulates lactation
  • Breast development
196
Q

What other pituitary hormones does prolactin inhibit

A

Inhibits GnRH from hypothalamus –> inhibits LH and FSH

197
Q

What are the signs and symptoms of prolactinoma (5)

A
  • Amenorrhea - no periods
  • Galactorrhoea - milky discharge
  • Gynaecomastia
  • Infertility
  • Bitemporal hemianopia
198
Q

How is prolactinoma investigated

A
  • Prolactin levels
  • MRI
199
Q

How is prolactinoma managed

A
  • Transphenoidal surgery
  • Medication
200
Q

What inhibits the production of prolactin

A

Dopamine

201
Q

What medication is used to treat prolactinoma

A

Dopamine agonists (bromocriptine) - inhibits prolactin, shrinks tumour

202
Q

What are some complications of prolactinoma (3)

A
  • Sight loss
  • Infertility
  • Raised ICP
203
Q

What are the two most common and other causes of hypercalcaemia

A
  • Hyperparathyroidism
  • Bone malignancies
  • Thiazide diuretics, hyperthyroidism, dehydration, high Ca2+ intake
204
Q

What may happen to the ECG trace in those with hypercalcaemia

A

Short QT segment

205
Q

What are the symptoms of hypercalcaemia (5)

A
  • Psyciatric moans
  • Abdominal groans
  • Painful boans
  • Kidney stones
  • Toiletry thrones
206
Q

What are the causes of hypocalcaemia

A
  • CKD (decreases vit d activation) - but can also cause hyper
  • Vit D3 deficiency
  • Drugs: calcitonin, bisphosphonates (slow bone loss)
207
Q

What is the affect of hypocalcaemia on ECG

A

Long QT segment

208
Q

What are the symptoms of hypocalcaemia

A
  • Convulsions
  • Arhythmias
  • Tetany
  • Numbness

CATs go NUMB

209
Q

Hyperkalaemia causes

A
  • Impaired secretion - AKI, CKD, low aldosterone, drugs
  • Increased intake
  • Shift to extracellular - acidosis, low insulin, sever burns
210
Q

Symptoms/ signs on hyperkalaemia

A
  • Fatigue
  • Arrhythmias
  • Weakness
  • Dyspnoea
211
Q

How is hyperkalaemia investigated

A
  • Bloods: U&Es
  • ECG
212
Q

What ECG findings would be present in hyperkalaemia (4)

A
  • No P wave (Go)
  • Long PR interval (Go Long)
  • Tall T wave (Go Tall)
  • Wide QRS complex (Go Wide)
213
Q

How is hyperkalaemia managed (4)

A
  • ABCs
  • Calcium gluconate - protects myocardium
  • Insulin + dextrose - moves K+ into cells, replaces glucose
  • Beta agonist (moves K+ into cells)
214
Q

Hypokalaemia causes

A
  • Increased excretion - CKD, increased aldosterone, D+V, drugs
  • Reduced intake
  • Shift to intracellular - alkalosis (K+ moves into cells so H+ can move out), drugs e.g. insulin, B2 agonists
215
Q

What are the signs/ symptoms of hypokalaemia

A
  • Arrhythmias
  • Fatigue/ weakness
  • Hypotonia
  • Hyporeflexia
216
Q

How is hypokalaemia investigated

A
  • Blood: U&Es
  • ECG
217
Q

How is ECG abnormal in hypokalaemia

A
  • Prolonged PR
  • ST depression
  • Prominent U wave
  • Inverted T wave
218
Q

How is hypokalaemia managed

A
  • IV potassium
  • Treat underlying cause
219
Q

How do beta-2 agonists affect K+

A

Increases activity of Na+/K+ ATPase pump therefore more K+ into cells

Na/k pump = 3 Na out; 2 K in

Phase 2a flashcards (Alec's) (13 decks)

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