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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
What investigations should be ordered for monitoring of diabetes?
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.
26
Who is on the MDT for a person with T2DM?
- GP - Diabetes educator - nutritionist/dietitian - Podiatrist - exercise physiologist
27
What lifestyle changes are advisable for a person with T2DM?
- 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
28
What are the BGLs to aim for in a person with T2DM?
aim to keep BGLs between 4-7mmol fasting and 5-10mmol postprandial
29
what is the first line drug for hyperglycaemic control?
metformin
30
what drugs are second and third line?
1. sulfonylureas → glicazide 2. SGLT2 inhibitors → dapagliflozin 3. DPP-4 inhibitors → sitaglipitin
31
what drugs are 4th line?
1. TZDs → pioglitazone 2. acarbose 3. GLP-1 analogue → exenatide, liraglutide 4. Insulin
32
what are the three main classes of drugs for diabetes and their brief MOA?
1. Sensitiers → increase tissue sensitivity to insulin 2. Increasers → drugs that increase insulin 3. Decreasers → drugs that lower Glucose
33
What is the MOA of sensitiers for Diabetes?
1. improve tissue response to insulin | 2. improves tissue utilisation of glucose, decreases liver production of glucose
34
What is the MOA of Increasers for Diabetes?
1. they act via various mechanisms to increase amount of insulin circulating
35
What are the 4 types of increasers?
1. sulfonureas 2. GLP-1 analgue 3. DPP-4 inhibitors 4. Insulin
36
What is the mechanism of action of Sulfonureas?
- stimulate release of insulin from the pancreas
37
What are examples of sulfonureas?
1. Gliclazide 2. glibenclamide 3. glipizide 4. glimepiride
38
What are some examples of GLP-1 analogues?
* Glutides* 1. dulaglutide 2. exenatide 3. liraglutide 4. semaglutide
39
What is the MOA and side effects of Dpp-4 inhibitors?
``` inhibits DPP-4 enzyme → increases amount of circulating incretins → increases insulin → decreases glucose. Side effects: - hypoglycaemia - headache - muscle pain ```
40
What are examples of DPP-4 inhibitors?
sitaglipine
41
What is the MOA and Side effects of insulin?
- enhances cellular uptake of glucose - inhibits gluconeogenesis and lipolysis SIDE EFFECTS: - hypoglycaemia - weight gain - allergic reactions
42
What are the two types of decreasors ?
1. SGLT-2 inhibitors | 2. Acarbose
43
What is the MOA and Side effects of SGLT-2 inhibitors?
- inhibits kidney reabsorption of glucose - weight loss Side effects: - Diuresis, UTI, DKA
44
What are some examples of SGLT-2 inhibitors
the Gliflozins - Dapagliflozin - empagliflozin
45
What is the MOA and SE of Acarbose?
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
What are two examples of sensitiers?
1. metformin | 2. Thiazolidinediones (TZDs)
47
What is the MOA and SE of metformin?
``` - increases tissue sensitisation to insulin to increase glucose uptake SE: - weight loss - GIT upset very common - Rare -> lactic acidosis ```
48
What is the MOA, SE and an example of TZDs?
``` 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
What is an acute complication of T2DM?
Hyperosmolar hyperglycaemic state
50
What is the pathogenesis of HHS?
- 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
What are the causes of HHS?
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
Investigations for HHS?
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
What complications can HHS cause?
- higher mortality than DKA - aspiration risk - pre-exisiting trigger can be cause of death - cerebral oedema - AKI
54
What is the management of acute HHS?
- Fluid resus ASAP - Iv insulin - potassium replacement
55
What is the pathogenesis of macrovascular complications of diabetes and the 3 types of complications
- 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
What is the pathogenesis of the mircovascular complications of T2DM and examples
- 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
What are the 2 main presentations of diabetic nephropathy?
- glycation of the glomeruler asement membrane -> progressive glomeruler hypertrophy -> glomerulosclerosis 1. Hypertension 2. proteinuria
58
What are the three main presentations of diabetic neuropathy?
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
Describe the presentation of retinopathy (2) and why it occurs
- due to microangiopathy results in two types of retinal disease 1. non-proliferative -> microaneurysms and cotton-wool spots 2. proliferative -> preretinal neovascularisation -> glucoma
60
What are the signs and symptoms of HHS?
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
what are common causative bacteria of UTI? (KEEPS)
- Klebsiella - E.coli → 80% - Enterobacter - proteus - staphlococcus saprophyticus → 10%
62
what are signs in examination of a UTI?
- tenderness in suprapubic and flank regions - renal angle tenderness - delirium or confusion in elderly - urine character → malodorous, cloudy, visible haematuria
63
what are symptoms of UTI?
- urinary frequency, urgency and dysuria - haematuria - fever/malaise - nausea and vomiting
64
what investigations to perform on the Urine for UTI?
- 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
What are modifiable risk factors for hyperthyroidism?
- Smoking - high iodine intake - lithium therapy - stress - pregnancy
66
What are non-modifiable risk factors for hyperthyroidism?
- Female gender - FHx of Autoimmune thyroid disease - previous radiation
67
what are the two most common categories of aetiological conditions that cause thyrotoxicosis?
1. hyperfunctioning thyroid gland -> overproduction of thyroid hormone 2. destruction of thyroid gland -> inappropriate release of stored thyroid hormone
68
What are 5 examples of conditions that cause hyperfunctioning thyroid gland?
1. grave's disease 2. toxic multinodular goitre 3. toxic adenoma 4. TSHoma 5. congential hyperthyroidism
69
What are 4 examples of conditions that destroy the thyroid gland resulting in Thyrotoxicosis?
1. De Quervain's thyroiditis 2. Postpartum thyroiditis 3. Drug induced 4. Hashitoxicosis
70
How does excessive circulating thyroid hormone effect the body?
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
What are signs of examination of hyperthyroidism?
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
What are symptoms of hyperthyroidism?
- 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
What is the pathophys behind the specific grave's disease clinical features? (exophthalmos and pretibial myxoedema)
- Grave's autoantibodies stimulate fibroblasts to secrete GAGs (hyalouronic acid) in some tissues which exerts an osmotic effect
74
What are specific manifestations of Grave’s disease and their pathophys?
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
What are the bedside, bloods and bichem investigations for hyperthyroidism and what results would you expect?
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
What are 2 imaging methods to assess thyroid gland for hyperthyroidism?
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
What treatment do all symptomatic hyperthyroid patients need to be given and why?
- beta blockers eg propranolol | - manage hyperadrenergic symptoms and decrease risk of cardiac complications eg AF
78
What are the three definitive options for treatment of Hyperthyroidism?
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
What are modifiable risk factors for hypothyroidism?
1. iodine deficiency → most common cause in developing world 2. treatment for hyperthyroidism 3. amiodarone and lithium use 4. pregnancy
80
What are non-modifiable risk factors?
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
What are the 4 main aetiologies of primary hypothyroidism?
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
what is the pathophysiology behind the clinical features of hypothyroidism?
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
What are the signs on examination of hypothyroidism?
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
What are symptoms of hypothyroidism?
- fatigue - cold intolerance - weight gain with poor appetite - constipation - depression - abnormal menstrual cycle
85
What is a myxoedema coma?
- medical emergency - caused by decompensation of thyroid hormone deficiency triggered by infection, surgery, trauma - presents with impaied cognition, hypothermia, myxoedema, hypoventilation or shock
86
What indicator is used for newborn screening of Hypothyroidism?
TSH
87
What antibodies are used to diagnose hypothyroidism?
Anti-thyroglobulin, anti-thyroid peroxidase, anti- TSH receptor
88
What imaging is used to assess hypothyroidism?
- Radioactive iodine uptake test → decreased uptake in hypothyroidism - US of thyroid
89
what is the treatment for hypothyroidism?
- lifelong Hormone replacement with levothyroxine (synthetic T4) - dose titration to avoid hyperthyroid. - monitoring of TSH levels
90
Which cells is PTH secreted from and in response to what?
1. cheif cells of the parathyroid glands in response to a: - decrease in serum calcium - increase in serum phosphate
91
What is the function of PTH?
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
what is the pathogenesis and pathophys of primary HPT?
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
What is the pathogenesis and pathophys of secondary HPT?
- 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 2. Malnutrition 3. vit D def other causes → cholestasis, reduced sunlight, cirrhosis
94
what are the DDx of hypercalcaemia?
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
what are the clinical manifestations of CKD-MBD?
1. pathological fractures 2. bone pain 3. avascualr necrosis 4. proximal myopathy 5. children have short stature and skeletal disorders
96
What are the sequelae of CKD-MBD?
1. diminished bone strength and mineralisation 2. soft tissue and vascular calcification 3. accelerated progression of cardiovascular disease
97
What is the treatment for CKD-MBD?
1. correcting mineral abnormalities → especailly hyperphosphataemia - diet low in phosphorous - vit D replacement - calcimimetics - phosphate binders (sevelamer) 2. Dialysis 3. parathyroidectomy

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