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Endocrinology > Endo > Flashcards

Endo Flashcards

1
Q

Outline the pathology between TI and TII DM

A

Type I:
Autoimmune destruction of the pancreatic islet cells leading to rescued insulin
Low C-peptide

Type II:
Hyper secretion of insulin by depleted beta cell mass. Increasing insulin resistance.
C-pepetide high

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2
Q

Physiology of the pancreas in response to glucose

A 
Alpha cells = glucagon 
Beta cells = Insulin 
Glucose enters the beta cells via the GLUT-2  pathway. 
Insulin is released 
Binds to the insulin receptor on muscles
Moblises GLUT -4 to memebrane, glucose can enter the cell. 
Suppression of 
- Gluconeogenesis
- Lipolysos 
- Proteolysis 
- Ketogenesis
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3
Q

A patient presents to the GP surgery complaining of polydipsia, polyuria and recurrent infections.
You suspect DM. What investigations will you run?

A 
Urine dip 
Fasting plasma glucose 
Random plasma glucose 
HbA1c
FBC

Note
- Symtomatic + one elevated FPG (≥7.0) or RPG (≥11.1)

  • HbA1c FPG OGTT (2hr)
    Normal: ≤ 5.6% <5.6 <7.8
    Prediabetes: 5.7-6.4 5.6-7 7.8-11.0
    Diabetes: ≥6.5% ≥7 ≥11.1
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4
Q

Outline the cut offs for the diagnosis of DM for the following readings

  • HbA1c
  • FPG
  • OGTT
A

HBa1C

  • normal: <56%
  • prediabetes: 5.7-6.4%
  • diabetes: >6.5%

FPG

  • normal: <5.6
  • prediabetes: 5.6 - 7
  • diabetes: >7

OGTT

  • normal: <7/8
  • prediabetes: 7.8- 11.0
  • diabetes: >11.1
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5
Q

List the complications associated with diabetes

A

NEUROPATHY

  • Lipid preoccupation of myelin
  • Glove and stocking distribution

NEPHROPATHY

  • Mesangial expnasion and thickening of glomerular BM
  • Narrowing of the efferent renal artery
  • Glomerular sclerosis and thickening of the BM
  • Increased gaps in the podcytes and hyperfilteration.
  • Rx ACEi/ARB

RETINOPATHY

  • Occlusion
  • Leakage (loss of parasites
  • Rx photocoagulation

CV

  • Increase risk
  • BP control and statins
  • QRISK

ERECTILE DYSFUNCTION

INFECTION

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6
Q

Discuss the risk factors for diabetic foot

A 
PAD 
Peripheral neuropathy 
Callus 
Smoking 
HTN
Hypercholestrolaemia
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7
Q

Presentation and features of diabetic foot

A

Ulcers

  • painless punched out
  • loss of pulses
  • charcot foot

Neuropathic joints

Loss of sensation

Chronic

  • Rockerbottom sole
  • Claw toes
  • Loss of transverse arch
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8
Q

List the problems associated with diabetic eye disease

A

Cataracts
Retinopathy
Maculopathy
Glaucoma

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9
Q

Features of diabetic eye disease

A

Painless, gradual reduction of central vision.

Microaneurysm 
Hard exudates 
Haemorrhages ( small dots, blots or flame) 
Cotton wool spots 
Neovascularisation

Dx on slit lamp test

Rx Laser photocoagulation

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10
Q

Classify the types of diabetic eye disease

A

Background retinopathy

  • Dots
  • Blots
  • Hard exudates (yellow lipid patches)

Pre-proliferative

  • Cotton wool spots (infarcts)
  • Venous bleeding
  • Dark haemorrhages
  • Intra retinal microvascular abnormalities

Proliferative

  • New vessels
  • Pre-retinal or viterous haemorrhage
  • Retinal detachment

Maculopathy

  • caused macula oedema
  • reduced acuity
  • hard exudates w/i one disc width of the macula
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11
Q

Outline the criteria for metabolic syndrome

A
  1. Truncal obesity
  2. HTN
  3. High triglycerides
  4. Fasting glucose >6.1mmol/L (prediabetes)
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12
Q

List the medications that can cause gynaecomastia

A 
Digoxin 
Isoniazid 
Spironolactone 
Cimetidine 
Oestrogen 
Steriods 
Finasteride
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13
Q

Conditions linked with gynaecomastia

A

Androgen resistance
Klinefleters
Mumps
Renal disease

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14
Q

Causes of hypothyroidism

A

PRIMARY

  • atrophic thyroiditis
  • hashimotos thyroiditis
  • post de quervains (painful qoitre raised ESR)
  • iodine deficiency
  • drugs ( carbimazole, amiodarone, lithium)

POST SURGICAL

SECONDARY
- hypopituitarism

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15
Q

Features of atrophic thyroiditis

A

Thyroid abs +ve, anti TPO, anti TSH
Atrophy no goitre
Assoc pernicious anaemia, vitiligo, endocrinopathies

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16
Q

Features of hashimotos

A

TPO+ve anti TG +ve
Atrophy and regeneration = goitre
Initial thyroidtoxicosis phase

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17
Q

A patient presents to you complain of feeling tired all the time, heavy period and constipation. She says it is getting her down.
O/E you notice she feels cold to touch, with a decrease HR, and slow reflexes.
What is your working dx?
What test will you order?
What will they show?

A
  1. Hypothyroidism
  2. TFT
    - Increase TSH
    - Decreased T3/T4
    - ? normochromic anaemia and increased MCV
    - SIAD ( if secondary)
    - Increase CK if myopathy
    - Abs: TPO, TSH
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18
Q

Treatment of hypothyroidism

A

Levothyroxine

  • titre to normalise TSH
  • 2 wks before improvement
  • beware of other autoimmune disease
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19
Q

Features of myxoedema coma

A 
Hypothermia 
Hypoglycaemia 
Heart failure (bradycardia with raised JVP)
Coma 
Seizures
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20
Q

Triggers for a myxoedema

A 
Radioiodine 
Thyroidectomy 
Pituitary surgery 
Infection 
Trauma
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21
Q

Treatment of a myxoedema coma

A
  1. Bloods
    - TFTs, FBC, U+E, glucose, cortisol
  2. Give T3/T4 IVI slowly
  3. Hydrocortisone 100mg IV
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22
Q

Causes of hyperthyroidism

A
  1. Grave’s disease
  2. Toxic multinodular goitre
  3. Toxic adenoma
  4. Toxic phase of thyroiditis
  5. Drugs
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23
Q

Features specific to Grave’s disease

A

Opthalmopathy

  • exophthalmos
  • ophthalmoplegia
  • eye discomfort/ grittiness
  • photophobia
  • decreased acuity
  • chemosis

Dermopathy
- pre-tibial myoxedema

Thyroid acropachy

Diffuse goitre

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24
Q

A patient presents to his GP surgery complain of weight loss despite an increased appetite, feeling sweaty and anxious with palpitations. She is worried she has got bad menopausal symptoms a she has not had a period in three months.
What do you suspect is the dx?
What investigations would you do?

A

TFTs

  • decreased TSH, increased T3/T4
  • abs: TSH receptor, TPO
  • increased Ca
  • increased LFTs

Eye screening

Radioiodine uptake scan

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25
Q

Treatment of patients with hyperthyroidism

A

Two methods

  1. Block and replace
  2. Dose titration

MEDICAL
Symptom relief: Beta blockers ( propanolol 40mg/6hr)
Block: Carbimazole (inhibits TPO)
(Graves disease treat for 12-18mnth and then withdraw and check if remission)
BEWARE OF AGRANULOCYTOSIS

RADIO-IODINE
- often become euthyroid

SURGERY
- thyroidectomy

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26
Q

Features of thyroid storm

A 
Increase temp 
Agitation, confusion, coma 
Tachycardia 
AF 
Acute abdomen 
Heart failure
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27
Q

Treatment of thyroid storm

A
  1. Fluid resuscitation + NGT
  2. Bloods: TFT’s + cultures if infection suspected
  3. Propranolol PO/IV
  4. Digoxin
  5. Carbimazole ( must give lug’s Iodine 4h later to inhibit the thyroid)
  6. Hydrocortisone
  7. Rx cause
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28
Q

Presentation of hyperparathyroidism

A 
(same as hypercalcaemia) 
Stone
- renal stones
- polyuria/ polydipsia
- nephrocalcinosis

Bones

  • Bone pain
  • pathological #

Moans
- Depression

Groans

  • Abdo pain
  • n/v
  • Constipation
  • Pancreatitis
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29
Q

Causes of hyperparathyroidism

A

Primary

  • Solitary adenoma
  • Hyperplasia
  • Pathyroid Ca
  • Association with MEN 1/2

Secondary

  • Vit D deficiency
  • Chronic renal failure
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30
Q

Outline the biochemical pictures seen in both primary and secondary hyperparathyroidism

A 
PRIMARY 
Increased Ca
Increased PTH 
Increased ALP
Decreased PO4

ECG: bradycardia, decreased QTc (1st degree block)

DEXA: osteoporosis

SECONDARY 
Increased PTH 
Decreased Ca 
Increased Po4 
Increased ALP 
Decreased Vit D
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31
Q

Treatment of primary hyperparathyroidism

A

General

  • increase fluid intake
  • avoid dietary Ca2+ and thiazides

Surgical excision of the adenoma

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32
Q

Treatment of secondary hyperparathyroidism

A 
Correct the causes 
Phosphate binders
- with Ca: calcite
- w/o : sevelamer 
Vitamin D: calcitriol ( active) 
Cinacalcet: increased PTH Ca sensitivty
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33
Q

Clinical features of hypoparathyroidism

A 
(SPASMODIC)
Spasms 
Perioral paraesthesia
Anxious 
Seizures 
Muscle tone increase 
Orientation impaired 
Dermatitis 
Impetigo herpetiformis (Ca + pustules)
Chovsteks, cardiomyopathy  ( Increased QTc)
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34
Q

Causes of hypoparathyroidism

A 
Autoimmune 
Congenital: DiGeorge 
- Cardiac abnormality 
- Abnormal facies 
- Thymic aplasia 
- Cleft palate 
- Hypocalcaemia 
- Chr 22

Iatrogenic

  • Surgery
  • Radiation
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35
Q

Treatment of hypoparathyroidism

A

Calcium and Vit D supplement

Recombinant PTH

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36
Q

Discuss pseudohypoparathyroidism

A 
Failure of the target organ to response to PTH 
Present with symptoms of hypocalcaemia 
Low calcium 
High PTH 
Rx with calcium and calcitrol
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37
Q

Features of Cushing’s syndrome

A

Catabolic effects

  • Proximal myopathy
  • Striae
  • Bruising
  • Osteoporosis

Glucocorticoid effects

  • DM
  • Obesity

Mineralocorticoid

  • HTN
  • Hypokalaemia
38
Q

Discuss the differences between ACTH independent and ACTH dependent causes and features of Cushing’s syndrome

A

ATCH independent

  • Low ACTH due to -ve FB
  • no suppression with any dose of dex

Causes

  • Iatrogenic steriods
  • Adrenal adenoma/ Ca
  • McCune Albright

ACTH dependent

  • High levels of ACTH
  • Cushing’s disease ( bilateral adrenal hyperplasia due to piturity adenoma
  • Ectopic ACTH
39
Q

Investigations in patients with Cushing’s syndrome

A 
1st 24hr urinary free cortisol 
Late night serum or salivary cortisol 
Dexamethasone supression tests 
ACTH ( rapid degradation) 
DEXA scan
40
Q

Treatment for Cushing’s Syndrome

A

Cushing’s disease

  • Trans-sphenoidal excision
  • Adrenal adenoma (adrenelectomy)
  • Ectopic ACTH
41
Q

Discuss Nelson’s syndrome

A

Rapid enlargement of a pituitary adenoma
Bilateral adrenelectomy for Cushing’s syndrome
Presentation of bitemporal hemianopia
Hyperpigmentation

42
Q

Causes of acromegaly

A

Pituitary acidophil adenoma
Hyperplasia from GHRH secreting tumour
GH stimulates bone and soft tissue growth through Increased IGF1

43
Q

Symptoms of acromegaly

A 
Acroparaesthesia 
Amenorrhoea 
Decreased libido 
Headache 
Snoring
Sweating 
Arthralgia, backahce 
Carpal tunnel
44
Q

Signs on acromegaly

A

HANDS

  • Spade-like
  • Thenar wasting
  • Boggy sweaty palms
  • Increased skin fold thickness
  • Carpal tunnel (decreased sensation + thenar wasting_

FACE

  • Supraorbital ridges
  • Coarse face, wide nose and big ears
  • Macroglossia
  • Widely-spaced teeth
  • Goitre

Puffy, oily, darkened skin
Proximal weakness + arthropathy
Pituitary mass effects (bitemporal hemianopia)

45
Q

Complications of acromegaly

A

Endocrine

  • Impaired glucose tolerance
  • DM

Cardiovascular

  • Increased BP
  • LVH
  • Cardiomyopathy
  • Increase IHD
  • increased stroke

Neoplasia
- Increased risk of CRC

46
Q

Treatment for acromegaly

A

1st line
- Trans-sphenoidal excision

2nd line
- Somatostatin analogues (octreotide)

3rd line
- GH antagonist (pegvisomant)

4th line
- Radiotherapy

47
Q

Effects of cortisol

A 
Suppression of reproduction 
Suppression of immunity 
Suppression of digestion 
Supression of growth 
Mobilisation of sugars
48
Q

Outline the pathophysiology o hyperaldosteronism

A

Conn’s syndrome is one of the primary causes of hyperaldosteronism
Secretion of aldosterone independently of RAAS

49
Q

What is the action of aldosterone

A

Insertion of ENaC and ROMK to luminal membrane of DCT

50
Q

Causes of hyperaldosteronism

A 
Bilateral adrenal hyperplasia 
Adrenocortical adenoma ( Conn's syndrome)
51
Q

Presenting features of hyperaldosteronism

A
  1. Hypokalaemia (weakness, hypotonia, hyporeflexia)
  2. Paraesthesia
  3. Increased BP
  4. Metabolic acidosis ( secretion of H+ in exchange for K+)
52
Q

A patient present complaining of weakness and swelling of the ankles
O/E there is marked weakness 3/5 on both the upper and lower limbs bilateral. Hyporeflexia and hypotonia was noted. There was marked peripheral oedema up to the level of the shins.
You suspect he may be suffering from Conn’s syndrome? What investigation would you order and what might they show?
What is the main electrolyte imbalance?

A

Bloods

  • U&E’s : high or normal NA+
  • Low potassium

ABG
- Metabolic alkalosis

Aldosterone:renin ratio: raised in primary hyperaldosterone

ECG:

  • Flat inverted T waves
  • U waves
  • Depressed ST segement
  • Prolonged PR
  • QT intervals

CT/MRI of the adrenals

HYPOKALAEMIA
LOW POTASSIUM

53
Q

Outline the management of patients with hyperaldosteronism

A

Conn’s
1. Medical management prior to surgery ( 4/52 of spirolactone treatment)
2. Laparoscopic adrenalectomy
(only if it is unilateral)

BAH

  • Aldosterone antagonist
  • Spironalactone ( blocks aldosterone and testosterone)
  • Amiloride ( not a good option)
54
Q

Outline the causes and pathology of secondary hyperaldosteronism

A

Due to increased renin from the reduced renal perfusion

CAUSES

  • RAS
  • Diuretics
  • CCF
  • Hepatic failure
  • Nephrotic syndrome

NOTE
the aldosterone: renin ration is normal

55
Q

Classify the types of diabetes insipidus

A
  1. Cranial
    - Idiopathic
    - Congenital
    - Tumours
    - Trauma
    - Vascular (haemorrhage/ Sheehan’s syndrome)
    - Infection
    - Infilteration ( sarcoidosis)
  2. Nephrogenic
    - Congenital
    - Metabolic ( low hypokalamia, high calcium)
    - Drugs (lithium, vaptains)
    - Post obstructive uropathy
56
Q

A patient is brought into hospital complain of polydipsia and chronic thirst. She also mentions she is suffering from weakness and confusions. On examination she has a grossly distended bladder.
You suspect that she may be suffering from diabetes insidious. You bleed the end reg and they ask you to order the appropriate investigations.
What would they be and what would they show?

A

24hr urine collection: ( >3L is significant)
Urine osmolality: < 300Osm/kg (2{Na+K} + urea + glucose)
Serum osmolality: normal or high (sodium, calcium and potassium)
Urine dip: -ve for glucose
MRI pituitary/ hypothalamus

KEY TEST
Water deprivation test with desmopressin response

57
Q

Management of cranial and nephrogenic diabetes insidious

A

Cranial
- Desmopressin replacement

Nephrogenic

  • Ensure adequate fluid intake
  • Treat cause

If hypernatraemic
- Lower sodium either with dietary or thiazide + NSAIDs

58
Q

What is the clinical picture that presents with SIADH

A

Euvolaemic hypotonic hyponatremia with concentrated urine.

59
Q

List the possible causes of SIADH

A

Pulmonary process

  • Pneumonia
  • Lung cancer
  • Malignancy
  • Drugs

CNS

  • Head injury
  • SAH

Endo
- Hypothyroidism

Drugs

  • Cyclophosphamide
  • SSRI’s
  • CBZ
60
Q

Patients who are diagnosed with SIADH often present with hyponatraemia which does not respond to normal saline.
List the investigations you would order to dc this condition ?

A

Na: low <135
Serum osmolality: low <280
Urine osmolality: >100mOsm/kg (higher than plasma)
Urine Na: >high 30

Normal renal function and adrenal function
Serum sodium will not respond to normal saline infusion.

61
Q

Management of SIADH

A
  1. Acute (<48) + severe (<125)
    - IV hypertonic saline (3%)
    - Check Na every 2 hours
    - Rx cause
    - Give furosemide if at risk of fluid overload
  2. Chronic + severe
    - IV hypertonic saline
    - Vasopressin receptor antagonist 9tolvaptan)
    - + cause
    - furosemide

Beware of cerebral pontine myolysis

62
Q

Features of hypokalameia

A 
Muscle weakness 
Hypotonia 
Hyporeflexia 
Cramps 
Tentany 
Palpatations
63
Q

EGG findings of hypokalaemia

A 
Flattened/ inverted T waves 
Prominent U waves 
ST depression 
Long PR interval 
Long QT interval
64
Q

Causes of hypokalaemia

A

INTERNAL DISTRUIBTION

  • Alkalosis
  • Increased insulin
  • B-agonist

EXCRETION

  • GI: vomiting
  • Renal: RTA
  • Drugs: Diuretics and steroids
  • Endo: Conn’s / Cushing’s
65
Q

Management of hypokalaemia

A

MILD >2.5

  • oral supplements
  • > 80mmol/d

SEVERE <2.5

  • IV KCl cautiously
  • give centrally, can burn

Must ensure they are not Mg depleted
If they are the K will not corrected itself regardless of rx

66
Q

List the ECG findings for hyperkalaemia

A 
Tall tented T waves 
Flattend P waves 
Increased PR interval 
Widened QRS complex 
Can progress to VF
67
Q

Causes of hyperkalaemia

A

ARTEFACT

  • Haemolysis
  • Lecucocytosis
  • Drip arm
  • Thrombocytosis

INTERNAL DISTRUBITION

  • Acidosis
  • Decreased insulin
  • Digoxin posioning
  • Cell death
  • Burns

EXCERTION

  • Renal failure
  • Addison’s
  • Drug’s (ACEi, NSAIDs, Pottassium sparking diuretics)
68
Q

Management of hypoerkalaemia

A

Non-urgent

  • Rx cause
  • Give calcium resinous, will lower K+ over several days

Urgent

  • > 6.5
  • 10ml of 10% Calcium Gluconate
  • 100ml of 20% glucose + 10u insulin
  • Salbutamol Nebs
  • Haemofilteration
69
Q

Outline the presentation of hyponatraemia according to it’s severity

A

<135: n/v, anorexia, malaise
<130: headache, confusion, irritable
<125: seizures, pul oedema
<115: coma and death

70
Q

Causes of hyponatraemia

A

HYPOVOLAEMIA

  • *UNa>20mm
  • Dieuretic
  • Addisons
  • Renal failure
  • *UNa<20mm
  • D/V
  • Fistula
  • SBO
  • Burns

HYPERVOLAEMIA

  • Cardiac failure
  • Nephrotic syndrome
  • Cirrosis
  • Renal failure

EUVOLAEMIC
- SIADH

  • Urine osmolality < 500
  • Fluid overload
  • Severe hypothyroid
  • Glucocorticoid insufficency
71
Q

Management of hyponatraemia

A
  1. Correct underlying cause
  2. Replace Na @ same rate lost
  3. Replace Na slowly, beaware of central pontine myeliolysis

URGENT
Hypoetonic saline solution 1.8%

72
Q

Features of hypernatraemia

A 
Thirst 
Lethargy 
Weakness
Irritability 
Confusion 
Fits 
Signs of dehydration
73
Q

Causes of hypernatraemia

A

HYPOVOLAEMIA
GI loss
Renal loss
Skin (burns)

EUVOLAEMIA
Decreased fluid intake

HYPERVOLAEMIA
Hyperaldosteronism
Hypertonic saline

74
Q

Management of hypernatraemia

A
  1. Give H2O orally if possible
  2. Give 5% dextrose IV or 0.9% NaCl if hypovolaemic
  3. Rehydrate slowly, beware of cerebral oedema
75
Q

Presentation of hypocalcaemia

A 
Spasms 
Perioral paraesthsia
Anxious. irritable 
Seizures 
Muscle tone 
Orientation 
Dermatitis 
Impertigo hepatoformis 
Chovsteks
76
Q

Causes of hypocalcaemia

A

Low PO4

  • CKD
  • HoPTH
  • Low Mg
  • Acute rhabdomyelsis

Normal PO4

  • Osteomalacia
  • Active pancreatitis
  • Resp alkalosis
77
Q

Features of hypocalcaemia

A

Stone

  • Renal stones
  • Polyuria
  • Polydispsia
  • Nephrocalcinosis

Bones

  • Bone pain
  • Pathological #

Moans

  • Depression
  • Confusion

Other

  • High BP
  • Decreased OT interval
78
Q

Causes of hypercalcaemia

A

Raised PO4 and raised ALP

  • Bone mets
  • Sarcoidosis
  • Thyrotoxicosis
  • Lithium

Rasied PO4 and normal ALP

  • Myeloma
  • High VITD
  • Sarcoidosis

Low PO4

  • Familial bengin hypercalcaemia
  • HPTH
  • Paraenoplastic (PTHrP)
79
Q

Management of hypercalcaemia

A

Rehydrate
- 0.9% NS over 4Hr 1L

If still high give bisphosphonates
Only use loop diuretics if fluid overload occurs

80
Q

List the causes of Addison’s

A 
Autoimmune destruction 
TB 
Metastasis (lung, breast, kidney)
Haemorrhage 
Congenital (CAH)
81
Q

Symptoms of Addison’s

A 
Weight loss 
Anorexia 
Nausea and vomiting 
Diarrhoea and confusion 
Depression 
Hyperpigmentation 
Postural hypotension 
Hypoglycaemia 
Vitiligo 
Addisonian crisis
82
Q

Investigations in patients with Addisonian symptoms

A

BLOODS

  • low NA
  • high K
  • low glucose
  • low Ca
  • Anaemia

High morning ATCH
Positive short synACTH test

21-hydroxylase Abs +ve
Plasma renin and aldosterone
CXR
AXR (adrenal calcification)

83
Q

Treatment for Addison’s

A

Replace

  • hydrocortisone
  • fludrocortisone

Advice

  • don’t stop steroids suddenly
  • wear a med-alert bracelet
84
Q

List the causes of secondary adrenal insufficiency

A

Chronic steroid use (suppression of the HPA axis)
Pituitary apoplexy/ Sheehan’s
Microadenoma

85
Q

Treatment of hypocalcaemia

A

Ca 5mmol QDS

Severe
10ml of 10% calcium gluconante over 10 mins

86
Q

Mechanism of action of Metformin

A

Increase insulin sensitivity (GLUT4)
Reduce gluconeogenesis
CI CKD/RF

87
Q

Mechanism of action of Gliptin

A

DPP4 inhibitor
Increases the levels of incretin
Increases the levels of insulin when needed

88
Q

Mechanism of action of Sulfonylurea

A

Oral hypoglycaemics
Increases the pancreas secretion of insulin
CI Pregnancy

89
Q

Mechanism of action of Pioglitazone

A

Increase insulin sensitivity
Rare risk of Bladder carcinoma
CI Heart failure (causes fluid retention)

90
Q

Mechanism of action of SGLT 2 inhibitors

A

Prevent the kidneys from absorbing glucose back into the blood stream

Endocrinology (2 decks)

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