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Phase 2 > Endocrine Medicine Topics > Flashcards

Endocrine Medicine Topics Flashcards

1
Q

describe the pathogenesis of T1DM

A
  1. autoimmune disease with unclear aetiology
    1. combination of genetic susceptibility (immune genes involved)
    2. and environmental triggers ( suggested to include viral infection and diet)
  2. Is a type IV hypersensitivity and autoimmune response with autoreactive T cells directed against Beta cells in the pancreatic islets
  3. results in progressive destruction of 80-90% of beta cells
  4. causes an absolute insulin deficiency → leads to hyperglycaemia
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2
Q

what are the typical signs and symptoms of T1DM? (6)

A
  1. secondary nocturnal enuresis (children)
  2. irritability
  3. classical triad of → polyuria, polydipsia and weight loss
  4. polyphagia
  5. fatigue and lethargy
  6. blurred vision
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3
Q

what are the typical signs and symptoms of diabetic ketoacidosis? (6)

A
  1. dehydration
  2. delirium or psychosis
  3. rapid breathing → kussmal in children
  4. abdominal pain
  5. nausea and vomiting
  6. ketonic fruity breath
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4
Q

what investigations to order to confirm diagnosis of T1DM? and what are the results of those tests?

A
  1. Random plasma glucose
    • must be >11.1mmol/L
  2. Fasting plasma glucose
    • must be > 7.0mmol/L
  3. 2- hour Oral Glucose Tolerance Test
    • > 11.1mmol/L
  4. HbA1c
    • > 6.5%
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5
Q

what additional tests can be ordered to distinguish between T1DM and T2DM?

A
  1. Islet autoantibodies
    • present in type 1
  2. C-peptide levels -> indirect measure of insulin levels
    • high suggests T2DM
    • low suggests T1DM
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6
Q

What are the different modes of insulin delivery?

A
  • Subcut delivery using needle or continuous pump
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7
Q

What is a typical insulin regime?

A
  1. basal insulin
  2. bolus insulin pre meal to account for cabohydrate levels
  3. supplemental insulin bolus to correct for abnormal BGL readings
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8
Q

What are the 5 key components in the long term management of a patient with T1DM?

A

Involvement of MDT
1. Patient education -> insulin dosing, diet, recognition and prevention of complications
2. Blood glucose monitoring -> goal 4-7mmol
3. Ketone monitoring -> when unwell or hyperglycaemic
4. HbA1c monitoring -> goal <7%
5 Diet

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9
Q

What is the pathogenesis of DKA?

A

Acute insulin deficiency

  1. Hyperglycaemia → osmotic diuresis → hypovolaemia and electrolyte derangement
  2. uninhibited lipolysis → increase in FFAs → increase in ketogenesis → ketosis and anion gap metabolic acidosis
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10
Q

what are the clinical features of DKA?

A
  1. classical diabetes triad
    • polyuria
    • polydipsia
    • weight loss
    • nausea and vomiting
  2. abdominal pain
  3. neurological changes
    • altered consciousness
    • lethargy
    • coma
  4. Kussmaul breathing
    • long deep breaths due to metabolic acidosis
  5. Fruity odour on breath from exhaled acetone
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11
Q

What is the diagnostic criteria of DKA?

A
  1. Hyperglycaemia
    • BGL > 11mmol/L
  2. Ketosis
    • presence of ketonemia or ketonuria
  3. Metabolic acidosis
    • VBG:
      • pH <7.3
      • bicarbonate < 15mmol/L
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12
Q

Describe the 4 key steps in management of DKA

A
  1. ABCDE assessment including hydration status
  2. IV fluid rehydration
    • normal saline used initially
    • KCl added as potassium begins to drop
    • 5% dextrose added when serum glucose begins to fall
  3. IV insulin infusion
    • corrects hyperglycaemia, ketosis and acidosis
  4. Ongoing monitoring for complications
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13
Q

what can cause insulin induced hypoglycaemia?

A
  1. incorrect insulin dosage
  2. variation in diet
  3. cessation of hyperglycaemic drugs
  4. exercise
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14
Q

what are the two categories clinical features can be classed as?

A
  1. adrenergic

2. neuroglycopenic

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15
Q

what are the adrenergic symptoms of IIH?

A
  • pale skin
  • sweating
  • shaking
  • tremor
  • palpitations
  • anxiety
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16
Q

what are the neuroglycopenic symptoms of IIH?

A
  • hunger
  • confusion
  • loss of consciousness
  • seizures
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17
Q

What s the treatment of non-severe and severe IIH?

A 
non-severe
- oral fast acting glucose
- oral fast acting carbs
Severe
- IV dextrose 10%
- IM glucagon
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18
Q

what are some modifiable risk factors for T2DM?

A
  1. obesity
  2. physical inactivity
  3. poor diet
  4. stress
  5. smoking
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19
Q

what are non-modifiable risk factors for T2DM?

A
  1. increased age
  2. family history
  3. non-white ancestry
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20
Q

Describe the two main mechanisms behind the pathophysiology of T2DM

A
  1. Peripheral insulin resistance
    • genetic and environmental factors result in impaired insulin dependent glucose uptake into the liver, muscle and fat tissue
  2. Pancreatic beta cell dysfunction
    • initially the endocrine pancreas is capable of compensating for insulin resistance
    • however, this capacity decreases over time as beta cells lose their secretory capacity
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21
Q

Briefly describe the progression to diabetes from normal physiology

A

normal → prediabetes with impaired glucose tolerance and isolated postprandial hyperglycaemia → diabetes with fasting hyperglycaemia

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22
Q

what are the signs of T2DM? (not chronic complications)

A
  • poor wound healing
  • recurrent infections
  • signs of insulin resistance → acanthosis nigracans, skin tags and hirsutism
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23
Q

what are some symptoms of T2Diabetes (not chronic complications)

A
  1. polyuria
  2. polydipsia
  3. lethargy
  4. blurred vision
  5. loss of sensation
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24
Q

what are the 4 key tests used to diagnose T2DM?

A
  1. Random plasma glucose
    • must be >11.1mmol/L
  2. Fasting plasma glucose
    • must be > 7.0mmol/L
  3. 2- hour Oral Glucose Tolerance Test
    • > 11.1mmol/L
  4. HbA1c
    • > 6.5%
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25
Q

What investigations should be ordered for monitoring of diabetes?

A
  1. HbA1c
  2. Lipids
    • LDL-c, HDL-c, total cholesterol, Triglycerides
  3. UECs
    • eGFR → monitoring nephropathy
  4. UA
    • looking for glycosuria
    • proteinuria as assessment of kidney function and or damage.
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26
Q

Who is on the MDT for a person with T2DM?

A
  • GP
  • Diabetes educator
  • nutritionist/dietitian
  • Podiatrist
  • exercise physiologist
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27
Q

What lifestyle changes are advisable for a person with T2DM?

A
  • increasing level of physical activity
    • weight loss and improving insulin sensitivity
  • weight loss → aggressive → bariatric surgery an option
  • smoking cessation
  • alcohol reduction
  • balanced nutritious diet
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28
Q

What are the BGLs to aim for in a person with T2DM?

A

aim to keep BGLs between 4-7mmol fasting and 5-10mmol postprandial

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29
Q

what is the first line drug for hyperglycaemic control?

A

metformin

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30
Q

what drugs are second and third line?

A
  1. sulfonylureas → glicazide
  2. SGLT2 inhibitors → dapagliflozin
  3. DPP-4 inhibitors → sitaglipitin
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31
Q

what drugs are 4th line?

A
  1. TZDs → pioglitazone
  2. acarbose
  3. GLP-1 analogue → exenatide, liraglutide
  4. Insulin
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32
Q

what are the three main classes of drugs for diabetes and their brief MOA?

A
  1. Sensitiers → increase tissue sensitivity to insulin
  2. Increasers → drugs that increase insulin
  3. Decreasers → drugs that lower Glucose
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33
Q

What is the MOA of sensitiers for Diabetes?

A
  1. improve tissue response to insulin

2. improves tissue utilisation of glucose, decreases liver production of glucose

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34
Q

What is the MOA of Increasers for Diabetes?

A
  1. they act via various mechanisms to increase amount of insulin circulating
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35
Q

What are the 4 types of increasers?

A
  1. sulfonureas
  2. GLP-1 analgue
  3. DPP-4 inhibitors
  4. Insulin
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36
Q

What is the mechanism of action of Sulfonureas?

A
  • stimulate release of insulin from the pancreas
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37
Q

What are examples of sulfonureas?

A
  1. Gliclazide
  2. glibenclamide
  3. glipizide
  4. glimepiride
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38
Q

What are some examples of GLP-1 analogues?

A
  • Glutides*
    1. dulaglutide
    2. exenatide
    3. liraglutide
    4. semaglutide
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39
Q

What is the MOA and side effects of Dpp-4 inhibitors?

A 
inhibits DPP-4 enzyme → increases amount of circulating incretins → increases insulin → decreases glucose. 
Side effects:
- hypoglycaemia
- headache
- muscle pain
40
Q

What are examples of DPP-4 inhibitors?

A

sitaglipine

41
Q

What is the MOA and Side effects of insulin?

A
  • enhances cellular uptake of glucose
  • inhibits gluconeogenesis and lipolysis

SIDE EFFECTS:

  • hypoglycaemia
  • weight gain
  • allergic reactions
42
Q

What are the two types of decreasors ?

A
  1. SGLT-2 inhibitors

2. Acarbose

43
Q

What is the MOA and Side effects of SGLT-2 inhibitors?

A
  • inhibits kidney reabsorption of glucose
  • weight loss
    Side effects:
  • Diuresis, UTI, DKA
44
Q

What are some examples of SGLT-2 inhibitors

A

the Gliflozins

  • Dapagliflozin
  • empagliflozin
45
Q

What is the MOA and SE of Acarbose?

A

MOA:
- prevents digestion of starch and thus absorption of glucose
- not as effective at reducing overall BGLs
SE:
- All GIT related
- gas, bloating, diarrhoea

46
Q

What are two examples of sensitiers?

A
  1. metformin

2. Thiazolidinediones (TZDs)

47
Q

What is the MOA and SE of metformin?

A 
- increases tissue sensitisation to insulin to increase glucose uptake
SE:
- weight loss
- GIT upset very common
- Rare -> lactic acidosis
48
Q

What is the MOA, SE and an example of TZDs?

A 
Piogliazone
MOA:
- binds to peroxisome in adipocytes to promote adipogenesis and fatty acid uptake
SE:
- weight gain
- peripheral oedema
- headache
atypical fractures in women
Contraindicated in Heart failure and bladder cancer
49
Q

What is an acute complication of T2DM?

A

Hyperosmolar hyperglycaemic state

50
Q

What is the pathogenesis of HHS?

A
  • uncontrolled hyperglycaemia causes osmotic diuresis and dehydration
  • presence of small amounts of insulin prevent ketones from being formed
  • can have metabolic acidosis from lactate
51
Q

What are the causes of HHS?

A
  1. medical assault on body -> acute sepsis, cardiovascular event, renal dysfuncion
  2. Insulin pump failure
  3. MI or unstable angine
  4. Trauma, surgery or burns
  5. Medications -> corticosteroids, atypical antipsychotics, immunosuppressives
  6. alcohol and recreational drugs
52
Q

Investigations for HHS?

A
  1. Bloods
    • BGLs → >15mmol
    • VBG → pH and bicarbonate
    • serum osmolality → elevated
    • CMP and EUCs → electrolyte disturbances
  2. Urinalysis
    • assess presence of ketones
    • specific gravity for level of dehydration aid.
53
Q

What complications can HHS cause?

A
  • higher mortality than DKA
  • aspiration risk
  • pre-exisiting trigger can be cause of death
  • cerebral oedema
  • AKI
54
Q

What is the management of acute HHS?

A
  • Fluid resus ASAP
  • Iv insulin
  • potassium replacement
55
Q

What is the pathogenesis of macrovascular complications of diabetes and the 3 types of complications

A
  • due to acceleration of atherosclerosis due to HTN, dyslipidaemia, hypercoaguability and vascular inflammation associated with diabetes and hyperglycaemia:
  • Cerebrovascular disease
  • Peripheral Vascular Disease
  • Cardiovascular/ Coronary artery disease
56
Q

What is the pathogenesis of the mircovascular complications of T2DM and examples

A
  • results from damage to small blood vessels due to processes of non-enzymatic glycation and sorbitol accumulation -> results in microangiopathy and damage to the retina, nephron and nerves:
    • retinopathy
    • nephropathy
    • neuropathy
57
Q

What are the 2 main presentations of diabetic nephropathy?

A
  • glycation of the glomeruler asement membrane -> progressive glomeruler hypertrophy -> glomerulosclerosis
    1. Hypertension
    2. proteinuria
58
Q

What are the three main presentations of diabetic neuropathy?

A
  1. Glove and stocking pattern of sensory loss in lower extremities
  2. Autonomic dysfunction
    - orthostatic HTN
    - erectile dysfunction
    - bladder dysfunction
    - loss of pupillary reflexes
    - gastroparesis
  3. Diabetic neuropathic arthropathy
    - charcot foot in severe diabetes
59
Q

Describe the presentation of retinopathy (2) and why it occurs

A
  • due to microangiopathy results in two types of retinal disease
    1. non-proliferative -> microaneurysms and cotton-wool spots
    2. proliferative -> preretinal neovascularisation -> glucoma
60
Q

What are the signs and symptoms of HHS?

A
  1. polydipsia
  2. polyuria
  3. lethargy
  4. marked dehydration
    • dry mouth, thirst, reduced urination
    • tachycardia
  5. nausea and vomiting
  6. neurological abnormalities
  7. seizure
  8. Do no get kussmaul breathing or weight loss
61
Q

what are common causative bacteria of UTI? (KEEPS)

A
  • Klebsiella
  • E.coli → 80%
  • Enterobacter
  • proteus
  • staphlococcus saprophyticus → 10%
62
Q

what are signs in examination of a UTI?

A
  • tenderness in suprapubic and flank regions
  • renal angle tenderness
  • delirium or confusion in elderly
  • urine character → malodorous, cloudy, visible haematuria
63
Q

what are symptoms of UTI?

A
  • urinary frequency, urgency and dysuria
  • haematuria
  • fever/malaise
  • nausea and vomiting
64
Q

what investigations to perform on the Urine for UTI?

A
  • Urine Dipstick
    • WBCs, nitrites (gram -ve bacteria eg e.coli), RBCs
  • Microscopy
    • presence of organisms
    • pyuria
    • haematuria
    • epithelial cells for contamination
  • Culture and sensitivity
    • ID of causative organism
    • sensitivity screen for targeted therapy
65
Q

What are modifiable risk factors for hyperthyroidism?

A
  • Smoking
  • high iodine intake
  • lithium therapy
  • stress
  • pregnancy
66
Q

What are non-modifiable risk factors for hyperthyroidism?

A
  • Female gender
  • FHx of Autoimmune thyroid disease
  • previous radiation
67
Q

what are the two most common categories of aetiological conditions that cause thyrotoxicosis?

A
  1. hyperfunctioning thyroid gland -> overproduction of thyroid hormone
  2. destruction of thyroid gland -> inappropriate release of stored thyroid hormone
68
Q

What are 5 examples of conditions that cause hyperfunctioning thyroid gland?

A
  1. grave’s disease
  2. toxic multinodular goitre
  3. toxic adenoma
  4. TSHoma
  5. congential hyperthyroidism
69
Q

What are 4 examples of conditions that destroy the thyroid gland resulting in Thyrotoxicosis?

A
  1. De Quervain’s thyroiditis
  2. Postpartum thyroiditis
  3. Drug induced
  4. Hashitoxicosis
70
Q

How does excessive circulating thyroid hormone effect the body?

A
  1. increased Na/K ATPase activity → increased BMR
  2. upregulation of beta adrenergic receptors → hypertimulation of SNS and hyperdynamic circulation
  3. decreased systemic vascular resistance
71
Q

What are signs of examination of hyperthyroidism?

A
  1. onycholysis
  2. lid lag and lid retraction → SNS overactivity → spasm of levator palpabrae superioris
  3. goitre
  4. tachycardia
  5. hypertension with wide pulse pressure
  6. fine tremour
  7. proximal myopathy
  8. hyperreflexia
72
Q

What are symptoms of hyperthyroidism?

A
  • heat intolerance and sweating
  • weight loss but increased appetite
  • diarrhoea
  • fatigue
  • palpitations and arrhythmias (AF)
  • oligomenorrhae or amenorrhae
  • erectile dysfunction and gynaecomastia
  • anxiety
  • restlessness
  • insomina
73
Q

What is the pathophys behind the specific grave’s disease clinical features? (exophthalmos and pretibial myxoedema)

A
  • Grave’s autoantibodies stimulate fibroblasts to secrete GAGs (hyalouronic acid) in some tissues which exerts an osmotic effect
74
Q

What are specific manifestations of Grave’s disease and their pathophys?

A
  1. opthalmopathy → GAG deposition in ocular muscles → causes expansion of retroorbital tissue
    • exopthalmos/proptosis
    • mobility disturbance leading to diplopia
  2. Pretibial myxoedema → GAG deposition within the legs
    • non-pitting oedema with an indurated appearance
75
Q

What are the bedside, bloods and bichem investigations for hyperthyroidism and what results would you expect?

A
  1. ECG
    • tachycardia, AF
  2. FBC
    • leukocytosis, mild anaemia
  3. TFTs
    • TSH, Free T4 and free T3
    • in graves, TSH low but T4 and T3 high
  4. Serology for TSH-R antibodies
    • present in graves
  5. UEC, CMP, BGL
    • hyperglycaemia, hypercalcaemia
  6. LFTs
    • may be mildly deranged
76
Q

What are 2 imaging methods to assess thyroid gland for hyperthyroidism?

A
  1. US + doppler
    • assess size of thyroid, nodules and any changes in perfusion
  2. Nuclear medicine thyroid scan → Scintigraphy
    • visualises the distribution of thyroid function within the gland
    • can identify hot/cold nodules and ectopic thyroid tissue
77
Q

What treatment do all symptomatic hyperthyroid patients need to be given and why?

A
  • beta blockers eg propranolol

- manage hyperadrenergic symptoms and decrease risk of cardiac complications eg AF

78
Q

What are the three definitive options for treatment of Hyperthyroidism?

A
  1. Antithyroid drugs → block thyroid peroxidase
    • carbimazole
    • propylthiouracil
  2. Radioactive Iodine Ablation (RAIA) → destruction of thyroid gland through radioactive isotope
    • usually used for Malignancy or Toxic MNG
    • patients become hypothyroid and need replacement
  3. Thyroidectomy
79
Q

What are modifiable risk factors for hypothyroidism?

A
  1. iodine deficiency → most common cause in developing world
  2. treatment for hyperthyroidism
  3. amiodarone and lithium use
  4. pregnancy
80
Q

What are non-modifiable risk factors?

A
  1. female sex
  2. middle age
  3. FHx of autoimmune thyroiditis or other autoimmune conditions
  4. Turner’s and Down’s syndromes
  5. radiotherapy to head and neck
81
Q

What are the 4 main aetiologies of primary hypothyroidism?

A
  1. Hashimoto’s thyroiditis → most common cause in developed world
    • autoimmune disease → Autoantibodies are produced to thyroid proteins and enzymes (antithyroid peroxidase, antithyroglobulin) → cause inflammatory destruction of the thyroid gland via infiltration of lymphocytes
  2. Iodine deficiency → most common cause in developing world
    • decreased iodine intake → essential component of thyroid hormones
  3. subacute thyroiditis → post-partum or de Quervains
    • typically initial thyrotoxic phase then hypothyroid phase due to damage to follicles
    • usually resolves after 6-8 weeks but can become permanent
  4. Iatrogenic
    • following hyperthyroidism treatment
    • amiodarone, lithium
82
Q

what is the pathophysiology behind the clinical features of hypothyroidism?

A
  1. Decreased BMR
  2. decreased Sympathetic activity
  3. myxoedema symptoms due to accumulation of GAGs in dermis → reduced thyroid hormone impairing noraml synthesis and degredation
  4. hyperprolactinaemia → stimulated by increase in TRH
83
Q

What are the signs on examination of hypothyroidism?

A
  1. bradycardia
  2. proximal myopathy
  3. carpal tunnel syndrome
  4. goitre
  5. delayed relaxation of reflexes
  6. hair loss, brittle nails and dry skin
  7. hyperprolactinaema → galactorrhae, gynaecomastia, infertility, amenorrhae, decreased libido
  8. Myxoedema → dough/puffy skin, horse voice, pretibial and periorbital oedema
84
Q

What are symptoms of hypothyroidism?

A
  • fatigue
  • cold intolerance
  • weight gain with poor appetite
  • constipation
  • depression
  • abnormal menstrual cycle
85
Q

What is a myxoedema coma?

A
  • medical emergency
  • caused by decompensation of thyroid hormone deficiency triggered by infection, surgery, trauma
  • presents with impaied cognition, hypothermia, myxoedema, hypoventilation or shock
86
Q

What indicator is used for newborn screening of Hypothyroidism?

A

TSH

87
Q

What antibodies are used to diagnose hypothyroidism?

A

Anti-thyroglobulin, anti-thyroid peroxidase, anti- TSH receptor

88
Q

What imaging is used to assess hypothyroidism?

A
  • Radioactive iodine uptake test → decreased uptake in hypothyroidism
  • US of thyroid
89
Q

what is the treatment for hypothyroidism?

A
  • lifelong Hormone replacement with levothyroxine (synthetic T4)
  • dose titration to avoid hyperthyroid.
  • monitoring of TSH levels
90
Q

Which cells is PTH secreted from and in response to what?

A
  1. cheif cells of the parathyroid glands
    in response to a:
    - decrease in serum calcium
    - increase in serum phosphate
91
Q

What is the function of PTH?

A
  1. Kidneys:
    • acts to increase calcium reabsorption and decrease phosphate reabsorption
    • increases vitamin D production in the kidneys
  2. Intestines:
    • Increases calcium absorption
  3. Bone:
    • releases calcium from the bones by increasing RANK-L expression on osteoblasts → which therefore results in increased osteoclast activity to reabsorb bone
92
Q

what is the pathogenesis and pathophys of primary HPT?

A
  1. increased PTH due primary disease in gland → benign adenoma (85%) or hyperplasia/multiple adenomas (15%), rarely lithium treatment
  2. High PTH levels:
    • increased bone reabsorption → release of calcium phosphate → hypercalcaemia and hypophosphataemia (due to PTH stimulation of phosphaturia)
93
Q

What is the pathogenesis and pathophys of secondary HPT?

A
  • Reactive increase in PTH secretion due to hypocalcaemia or hyperphospataemia
    • mostly due to vit D deficiency
      1. CKD is the most common cause
    • impairs Vit D synthesis → hypocalcaemia
    • decreased phosphate excretion → hyperphosphatemia
      1. Malnutrition
      2. vit D def other causes → cholestasis, reduced sunlight, cirrhosis
94
Q

what are the DDx of hypercalcaemia?

A
  1. any of the HPT disorders
  2. underlying cause of sHPT
    • CKD
    • cirrhosis
  3. malignancy
    • multiple myeloma
    • other haematological malignancy
    • paraneoplastic carcinomas
  4. medications
    • thiazide diuretics
  5. thyrotoxicosis
95
Q

what are the clinical manifestations of CKD-MBD?

A
  1. pathological fractures
  2. bone pain
  3. avascualr necrosis
  4. proximal myopathy
  5. children have short stature and skeletal disorders
96
Q

What are the sequelae of CKD-MBD?

A
  1. diminished bone strength and mineralisation
  2. soft tissue and vascular calcification
  3. accelerated progression of cardiovascular disease
97
Q

What is the treatment for CKD-MBD?

A
  1. correcting mineral abnormalities → especailly hyperphosphataemia
    • diet low in phosphorous
    • vit D replacement
    • calcimimetics
    • phosphate binders (sevelamer)
  2. Dialysis
  3. parathyroidectomy

Phase 2 (10 decks)

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