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MBBS VI Medicine > Endocrine system > Flashcards

Endocrine system Flashcards

1
Q

What is the classification of DM?

A

Type 1 DM
* Increased risk in patients with positve family history
* Presence of autoimmune antibodies: insulin (anti insulin antibodies), GAD, insulinoma associated protein 2: IA-2 antibodies, islet cell (ICA): anti-islet cell antibodies, zinc transporter (Zn T8 antibodies)
* Pathogenesis: T-cell mediated autoimmune destruction of pancreatic beta-cells = inadequate insulin secretion
Type 2 DM
* Onset later in life
* Pathogenesis: decreased sensitivity to insulin (insulin resistance), inadequate compensatory insulin secretory response (B cell dysfunction)
Latent autoimmune diabetes in adults (LADA)
* Apparent T2DM patients may have circulating autoantibodies against pancreatic B cell antigens
* On the spectrum of insulin deficiency between type 1 and type 2 diabetes
* Respond to treatment as in type 1 DM: less endogenous insulin production. Respond poorly to oral hypoglycemic agents, progress more quickly to insulin dependence.
Mature onset diabetes of the young (MODY)
* Monogenic diabetes with autosomal dominant inheritance. Non insulin dependent DM diagnosed at young age (<25 years): considered in young subjects with strong family history.
Gestational DM
* Insulin resistance mediated by placental secretion of diabetogenic hormones: human placental lactogen, progesterone, GH, corticotrophin releasing hormone (CRH)
* RF for GDM: advanced materna lagae >35 years old, medical history (maternal obesioty, maternal glycosuria), FH of DM, drug history of corticosteroids, OG history: multiple pregnancy, previous history of GDM, previous macrosomia, previous unexplained stillbirth or abnormal babies
Secondary DM
* Pancreatic disorders: pancreatitis, pancreatic tunmors, pancreatic haemochromatosis, pancreatic reseciton, cystic fibrosis (exocrine)
* Endocrine disorders: acromegaly (GH), cushing syndorme (cortisol), hyperthyroidism, glucagonoma (glucagon), phaeochromocytoma
* Drug induced: corticosterids, B blockers, thiazide diuretics, HIV medications, antipsychotics (1st gen: chlopromazine, 2nd gen: clozapine/quetiapine/risperidone)

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2
Q

Comparison between T1DM and T2DM
- Prevalence
- Age of onset
- Onset
- Body weight
- Family history
- TWin concordance
- Symptons
- Treatment
- Endogenous insulin
- Ketosis
- Human leukocyte antigen
- Autoantibodies

A
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3
Q

What are the RF and criteria for metabolic syndrome?

A
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4
Q

What are the genetic components of passing down T2DM?

A
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5
Q

What are the genetic and immune factors that cause T1DM?

A
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6
Q

What are the environmental stimuli and the mutations of genes regulating insulin secretion that contribute to T1DM?

A
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7
Q

How does obesity and lack of excercise lead to T2DM?

A
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8
Q

What is the normal insulin stimulated glucose transport
What is the effect of FA on glucose regatulation?

A
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9
Q

What are the consequences of obesity (FA on inducing hyperlipidemia) in T2DM?

A
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10
Q

What are the classical SS of DM?

A
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11
Q

What is the diagnostic criteria for DM?

A
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12
Q

What are the limitations of HbA1c in making a dx of DM?
Other conditions causing an increase or decrease in HbA1c

A
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13
Q

What are the antibodies/biochemical tests done for DM?

A
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14
Q

What is the insulin treatment for DM?

A
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15
Q

What is the clinical usage of human insulin and insulin analog?

A
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16
Q

What is the dosage of insulin for DM control in T1DM and T2DM?

A
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17
Q

What oral DM drugs increase insulin secretion
What are classes and examples. MoA and AE?

A
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18
Q

What oral DM drugs are incretin based
Increased insulin actions (insulin sensitizers)
What are classes and examples. MoA and AE?

A
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19
Q

What oral DM drugs decrease oral uptake
What drugs increase glucose excretion?
Class, examples, MoA and AE?

A

Risks of SGLTII
- Septicaemia due to UTI
- Euglycaemic ketoacidosis

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20
Q

Compare hypoglycemic agents in DM?
What is the treatment algorithm?

A
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21
Q

What are the treatment targets for DM?

A
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22
Q

What is the lifestyle modificiation for DM?

A
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23
Q

What are the complications of DM?

A
  • Diabetic ketoacidosis and ketotic coma: occurs in T1DM but also occurs in ketosis prone T2DM
  • Diabetic hyperosmolar hyperglyemic state (HHS) +/- non ketotic coma
  • Chronic complications
    Macrovascular: atherosclerosis, CAD, stroke, peripheral vascular disease
    Microvascular: neuropathy, nephropathy, retinipathgy
    Infections (immunosuppression): UTI, candidiasis, mucormycosis, osteomyelitis of the foot.
    Dermatological diseases: diabetic dermopathy, acanthosis nigricans, necrobiosis lipoidica diabeterticorum, lipodystrophy
  • Diabetic nephropathy
  • Diabetic retinopathy
  • Diabetic neuropathy
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24
Q

What is the pathogenesis of hyperglycemia in DKA, pathogenesis of ketosis in DKA
Precipitating factors of DKA
Clinical manifestation
Diagnostic criteria

A
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25
Q

What are the Ix for diabetic ketoacidosis
What parameters need to be monitored?

A
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26
Q

What is the treatment for diabetic ketoacidosis?

A

KING UFC

  • K+ (potassium supplementation)
  • Insulin
  • NG tube
  • Glucose (once serum levels drop)
  • Urea (monitoring kidneys)
  • Fluids
  • Creatinine (monitor)
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27
Q

What are the general features of diabetic hyperosmolar hyperglycemis states (HHS) +/-non ketotic coma
clinical manifestation
Precipitating factors of HHS
Diagnostic criteria
Treatment

A
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28
Q

What are the chronic complications of DM and when to screen?

A
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29
Q

What is the pathogenesis of diabetic nephropathy?

A
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30
Q

What is the histopathological features of DM nephropathy?
How to classify the severity

A
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31
Q

What Ix to make a dx of DM nephropathy?

A

Last line when uncertain (normally not necessary)
USG: structural and obstructive lesions, hydronephrosis, asessment of renal size
Renal biopsy: only if the the dx of diabetic nephropathy is uncertain

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32
Q

What is the management of DM nephropathy?

A
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33
Q

What are the general features of diabetic retinopathy
What can be the causes of visual loss?

A
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34
Q

What is the classification of DM retinopathy?

A
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35
Q

What is the clinical manifestation of DM retinopathy?

A

 Visual loss
* Macular edema
* Pre-retinal or vitreous hemorrhage (from neovascularization)
* Traction retinal detachment
* Neovascular glaucoma
 Floaters
* Retinal tear

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36
Q

What is the pathogenesis of DM retinopathy?

A
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37
Q

What are signs of visual loss in DM retinopathy?

A
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38
Q

What are signs seen in fundoscopy and fluorescein angiography for DM retinopathy?

A
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39
Q

What is seen in fundoscope for non proliferative DR?

A
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40
Q

What is seen in fundoscope for proliferative DR?

A
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41
Q

What is seen in fundoscope for proliferative DR with fibrous proliferation but no traction retinal detachment?

A
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42
Q

What is seen in fundoscope for proliferative DR with fibrous proliferation with traction retinal detachment?

A
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43
Q

What to observe for in fundoscopic examination of suspected DM retinopathy?

A
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44
Q

Apart from basic fundoscopy what other Ix may be done to look for complications of DM retinopathy?

A
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45
Q

What is the treatment for diabetic retinopathy?

A
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46
Q

What is done for prevention of DM retinopathy?

A
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47
Q

What is the clinical manifestation of diabetic neuropathy
How to assess severity of neuropathy?

A
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48
Q

What is most likely dx
What ix to perform

A
  1.  DM presenting with diabetic ketoacidosis (DKA)
     Differential diagnosis for a high anion gap acidosis (↑ H+)
    * Lactic acidosis
    * Salicylate overdose
    * Methanol poisoning
    * Neurological causes
    o Stroke
    o Head injury

2.
 Plasma glucose, ketones, electrolytes
 Urine ketones
 Blood-gas analysis
 Look for precipitating infections
* Respiratory
* Gastrointestinal
* Septicemia
* Meningitis

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49
Q

What is initial Mx
What is subsequent Mx
What advice to give patient to prevent future episode?

A

 Fluid replacement therapy with large volume of isotonic saline
* IV K+ replacement is likely to be required
* Polyuria will persist until glucose level is normalized
 IV Short-acting insulin
 IV bicarbonate (HCO3-)
* Only indicated in severe acidosis (pH > 7.0) since admission of alkali is associated with serious side effects such as hypokalemia and paradoxical acidosis of CSF
 Remarks
* Frequent monitoring of serum K+ and glucose level
* Central line is useful to guide therapy especially in elderly with concomitant cardiac
dysfunction
* Underlying infection should be treated

 Subcutaneous insulin injection
* After the patient is stabilized
 Diabetic education
* Need of insulin treatment and insulin self-administration
* Self-monitoring of BG
* Recognition and treatment of hypoglycemia

 Reinforcement of “sick-day rule”
* More frequent monitoring of BG and check urine or blood for ketones during illness
 Marked hyperglycemia requires temporary adjustment of insulin regimen
 Seek medical advice if hyperglycemia is accompanied by ketosis

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50
Q

Q1: What diabetic complications have developed in this patient?
Q2: What pathology may be found in the kidneys?
Q3: What investigations should be performed in the patient?

A
  1.  Diabetic nephropathy leading to fluid overload
    * Diabetic nephropathy is clinically defined by persistent proteinuria > 500 mg/ 24 hours (24-hour urine collection) in patient with DM without other renal disease
     Diabetic retinopathy
    * Dot and blot hemorrhages
     Ischemic heart disease
    * Suggested by presence of chest pain
    * Macrovascular complication of diabetes
  2.  Diabetic glomerulosclerosis
    * Consequence of ECM deposition in glomeruli
     Nodular glomerulosclerosis
    * Along with typical Kimmelstiel-Wilson nodules
     Mesangial cell expansion
     Arteriolar hyalinosis
    * Leads to ischemic changes

3.
 Assessment of renal function: CrCl (timed urine collection), eGFR using accepted equation
 Urinalysis: Performed to look for infection or hematuria
 Quantification of proteinuria
 USG kidneys: Assess renal size or morphology, exclude obstruction and other concomitant lesions

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51
Q

How should the BP be controlled?
What kinds of hypoglycemic drugs should be avoided in DM patients with renal failure

A

 BP control by
* ACEI/ ARI
* β-blocker
* CCB
* Diuretics
 Remarks
* Evidence shows beneficial reno-protective effect of using ACEI or ARB
* Hyperkalemia is a potential concern and should be monitored in these patients

Drugs that are partially excreted via kidneys (can cause hypoglycemia especially in elderly with reduced renal function) e.g. chlorpropamide
Biguanides: avoided since it can predispose to lactic acidosis in the presence of renal impairment

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52
Q

Define hypoglycemia in patients without DM and with DM

A
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53
Q

What is response to hypoglycemia in normal patients?

A
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54
Q

What is response to hypoglycemia in DM patients?

A
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55
Q

What are the causes of hypoglycemia in ill or medicated individuals as well as seemingly well individuals?

A
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56
Q

What are teh SS of hypoglycemia?

A
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57
Q

What is the general diagnostic approach for hypoglycemia?

A
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58
Q

What are the biochemical tests for hypoglycemia and why?

A
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59
Q

How to interpret the blood tests done for hypoglycemia and the diagnostic interpretation?

A
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60
Q

What are the imaging done for hypoglycemia (not routine)?

A
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61
Q

What is management of hypoglycemia?

A
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62
Q

What is the classification of diabetes insipidus?

A
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63
Q

What are the causes of central DI?

A
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64
Q

What are the causes of nephrogenic DI?

A
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65
Q

What is the ddx of DI?

A

 Solute or osmotic diuresis
* Glucose diuresis
o Uncontrolled DM
* Urea diuresis
o Tissue catabolism
o High-protein diet
* Sodium diuresis
o Normal saline infusion
o Bilateral urinary tract obstruction

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66
Q

What is serum osmolality
Where is ADH produced and secreted

A
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67
Q

What is MoA of ADH?

A
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68
Q

What SS for DI?

A

 Polyuria
* Defined as urine output > 3L/day in adults and > 2L/m2 in children
 Polydipsia
 Nocturia
* Urine is most concentrated in the morning due to lack of fluid ingestion overnight and increased ADH secretion during late sleep period
* First manifestation of a mild to moderate loss of concentrating ability is therefore nocturia

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69
Q

What history taking for DI?
What basic Ix?

A
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70
Q

What specific tests and procedure done for DI?

A
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71
Q

What is the treatment of central DI?

A
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72
Q

What is the treatment of nephrogenic DI?

A
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73
Q

What is the mnemonic for sequential loss of pituitary hormones?

A
  • GHS PTA = Good Hope School Parent-Teacher Association
    o GH = Growth hormone deficiency –>
    o S = Sex hormone (LH and FSH) deficiency –>
    o P = Prolactin –>
    o T = Thyroid hormone deficiency (Hypothyroidism) –>
    o A = ACTH deficiency
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74
Q

What are the hypothalamic disorders causing hypopituitarism?

A
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75
Q

What are the pituitary disorders causing hypopituitarism?

A
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76
Q

What are the SS of pituitary hormonal deficiency?

A
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77
Q

How to biochemically test for pitutiary hormony deficiency?

A
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78
Q

What is treatment for ACTH deficiciency?
TSH deficiency?

A
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79
Q

What is treatment of prolactin deficiency
gonadotrophin deficiency
GH deficiency

A
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80
Q

What is treatment of ADH deficiency?

A
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81
Q

How do you classify pituitary adenoma (size, functionality and cell origin)?

A
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82
Q

What is the prevalence of diffrent types of pituitary adenoma?

A
  • Lactotroph adenoma* >
  • Non-functioning adenoma (25 – 35%) >
  • Somatotroph adenoma >
  • Corticotroph adenoma
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83
Q

What is the ddx of sellar mass?

A
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84
Q

What is the anatomy of the sellar region and hypothalamic pituitary hormones?

A
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85
Q

What are the SS of pituitary adenoma?

A
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86
Q

What are the Ix done for pituitary adenoma?

A
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87
Q

What is the medical and surgical treatment for pituitary adenoma?

A
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88
Q

What is the physiological and pathological causes of hyperprolactinemia?

A
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89
Q

What is the pathogenesis of hyperprolactinemia induced hypogonadotrophic hypogonadism?

A
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90
Q

What are the SS of hypopituitarism in males and females?

A
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91
Q

What Ix are done for hyperprolactinemia?

A
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92
Q

What is medical and surgical treatment for hyperprolactinemia?

A
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93
Q

What is the process of thyroid hormone synthesis?

A
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94
Q

What is the mechanism of thyroid hormone action?

A
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95
Q

What is the physiological effect of thyroid hormones?

A
96
Q

What are the causes of thyrotoxicosis?

A
97
Q

What are the causes of hypothyroidism?

A
98
Q

What are the SS of hyperthyroidism?
What is scoring system for graves opthalmopathy?

A
99
Q

What are the SS of hypothyroidism?

A
100
Q

What are the classical features in general appearance, eyes and hands in thyrotoxicosis?

A
101
Q

What are the classifical features in arms, legs and neck of thyrotoxicosis?

A
102
Q

What are the classical features of hypothyroidism?

A
103
Q

What is the diagnostic protocal for thyrotoxicosis?

A
104
Q

What is the diagnostic protocal for hypothyroidism?

A
105
Q

What are ix done in thyroid disease?

A
  • CBC with DC: baseline to prep patient for thionamides which can cause agranulocytosis
  • LFT: baseline LFT to prep patient for thionamides which can cause hepatotoxicity
  • TFT: do not use TSH level to monitor response to treatment since it can remain suppressed for several months (use T3 and T4 level instead)
  • TSH: most sensitive indicator of thyroid function due to short t1/2
  • fT4 level, fT3 level
  • Thyroid antibdoies: anti TSH antibiodies, anti TPO antibdoies, anti TG (thyroglobulin) antibodies

Radiological
* Thyroid USG
* FNA if compatible with sonographic criteria
* Radionuclide scan (scintigraphy 99tc)

106
Q

What is the use of fT4 and fT3 level in thyroid disease?
Why is fT4 measured instead of total T4?

A
107
Q

What thyroid antibodies tested and are they specific to what diseases?

A
108
Q

What are USG findings that are high risk for thyroid cancer, low risk for thyroid cancer?

A
109
Q

What is the sonographic criteria for FNA in thyroid lesion?

A
110
Q

What are the indications for FNA for cytology in thyroid?
What classification of diagnostic categories are there? How does this guide management?

A
111
Q

What can a thyroid radionuclide scan show and how does it guide management?

A
112
Q

What treatment options are there for hyperthyroidism?

A
113
Q

What is short term treatment of hyperthyroidism?

A
114
Q

What is long term treatment of hyperthyroidism?

A
115
Q

What is the management of thyroid storm?

A
116
Q

What is treatment of hypothyroidism?

A
117
Q

What is the management of myxedema coma?

A
118
Q

Why is serum fT4 measured instead of total T4?

A

 Serum total T4 is a measurement of total T4 bounded to plasma binding proteins including thyroxine-binding globulin (TBG) and thyroxine-binding prealbumin (TBPA)
 Plasma binding proteins are affected by diseased state
* ↑ in pregnancy
* ↓ in hypoalbuminemia

119
Q

What are the preparations, contraindication and side effects for admin of radioactive iodine in thyroid disorder?

A
120
Q

What are the causes of acromegaly?

A
121
Q

What is the effect of increased GH?

A
122
Q

What are the direct local effects of pituitary tumor?

A
123
Q

What are the clinical features of GH/IGF1 excess?

A
124
Q

What are the 3 main Ix done for acromegaly?

A

Serum IGF-1 + OGTT (confirm if GH is not suppressible) + pituitary MI

125
Q

What are bedside basic tests to monitor progress of acromegaly?

A
  • Check ring size of the patient
  • X-ray heel for heel-pad thickness
126
Q

What is the medical treatment for acromegaly?

A
127
Q

What is the surgical management of acromegaly?
What are the indications for surgical intervention?

A
128
Q

How to classify cushing syndrome?

A
129
Q

What are the causes of cushing syndrome?

A
130
Q

What is the ddx and signs to look for in cushing syndrome?

A

 Signs that suggest adrenal tumour is the underlying cause
* Palpable abdominal mass
* Gynecomastia in males
* Virilization in female
 Signs that suggest ectopic ACTH production the underlying cause
* Absence of Cushingoid body habitus
* More prominent edema and hypertension
* More prominent muscle weakness

131
Q

What are the clinical features of cushing syndrome?

A
132
Q

What are the associated conditions with cushing syndrome?

A

 General conditions
* Hypertension (60 - 80%)
* Dyslipidemia (40 – 70%)
* Overweight/ Obesity (90%)
* Diabetes mellitus/ IGT (65%)
 CNS system
* Major depression and anxiety disorders (55 – 80%)
* Impaired memory
* Sleeping disturbance
* Psychosis
 MSS system
* Osteoporosis
* Proximal muscle weakness and wasting

133
Q

What is the protocal for investigations in suspected cushing syndrome?

A
134
Q

How to exclude physiological hypercortisolism in absence of CS?
What is the initial testing of CS?
Individuals with at least 1 abnormal test should undergo what further testing?

A
135
Q

What is done for screening and confirmation of cushing syndrome?
What tests done to establish the specific cause of CS?

A
136
Q

How is 1mg/low dose overnight dexamethasone suppression test (ONDST) done for cushing syndrome
Interpretation and limitations

A
137
Q

How is 24 hour urinary free cortisol done for cushing syndrome?
Interpretation and limitations

A
138
Q

How is late night salivary cortisol done for cushing syndrome?
Interpretation and limitations

A
139
Q

How is plasma ACTH measurement done for cushing syndrome?
Interpretation

A
140
Q

How is CRH stimulation test done for cushing syndrome?
Interpretation

A
141
Q

How is high dose (2mg) overnight dexamethasone suppression test (ONDST) done for cushing syndrome?
When is it used and interpretation

A
142
Q

How is bilateral inferior petrosal sinus sampling/catheterization (BIPSS) done for cushing syndrome?
Interpretation

A
143
Q

What are the different tests that can be done for differentiation of cushing syndrome?

A
144
Q

What is medical treatment of cushing syndrome?

A
145
Q

What is the treatment of primary adrenal diseases of cushing disease?

A
146
Q

What is treatment for cushings disease?

A
147
Q

What is the treatment (medical and surgical) of ectopic ACTH
syndromes
When indicated?

A
148
Q

What are the complications of cushing syndrome?

A
149
Q

What are the causes of primary hyperaldosteronism (conns syndrome)
and secondary hyperaldosteronism?

A
150
Q

What are the causes of non aldosterone mineralocorticoid excess for hyperaldosteronism?

A
151
Q

What adrenal hormone secreted and from which zone?

A

GFR MGS (salt, sugar, sex)

Zona glomerulosa (outer zone): mineralocorticoids (aldosterone)
Zona fasciculata (midle zone): glucocorticoids (cortisol)
Zona reticularis (inner zone): sex hormones (DHEAS)

Adrenal medulla –> epinephrine and norepinephrine

152
Q

What is the RAAS system
What stimulates RAAS
Aldosterone actions

A
153
Q

How is the synthessi of adrenocortical steroids done?

A
154
Q

What is the SS of hyperaldosteronism?

A
155
Q

What are the screening and confirmatory testing done for hyperaldosoteronism?

A

 Screening test
* Plasma aldosterone concentration (PAC)
* Plasma renin activity (PRA)
* Plasma aldosterone-to-renin ratio (ARR)
 Confirmatory test (one of the four test)
* Oral sodium loading test
* Saline infusion test
* Fludrocortisone suppression test
* Captopril challenge test

156
Q

How is hyperaldosteronism screened for
What interfering drugs will affect results
What is the interpretation of results

A
157
Q

What confirmatory tests are done for primary hyperaldosteronism and how to interpret the results

A
158
Q

How to differentiate between different causes of primary hyperaldosteronism?

A
159
Q

How to differentiate between adenoma and hyperplasia in hyperaldosteronism?

A
160
Q

What are the medical and surgical indications for primary hyperaldosteronism?

A
161
Q

What are the surgical options for primary hyperaldosteronism and the complications?

A
162
Q

How to classify adrenal insufficiency?

A
163
Q

What are the causes of primary adrenal insufficiency?

A
164
Q

What are the causes of secondary adrenal insufficiency?

A
165
Q

What are the causes of tertiary adrenal insufficiency?

A
166
Q

What are the causes of addisonian crisis?

A
167
Q

What are the different stages of autoimmune adrenalitis?

A

 Autoimmune adrenalitis is the most common cause of primary adrenal insufficiency which is a process that worsens over a period of many months or years
* Stage 1 = High plasma renin activity; Normal/ Low serum aldosterone
* Stage 2 = Impaired serum cortisol response to ACTH stimulation
* Stage 3 = Increasing morning plasma ACH with normal serum cortisol
* Stage 4 = Low morning serum cortisol and overt clinical adrenal insufficiency

168
Q

What is the clinical manifestation of addisonian crisis?

A
169
Q

What are the classical clinical manifestation and how to differentaite between primary and secondary/tertiary adrenal insufficiency?

A
170
Q

What are the basic and screening ix for primary adrenal insufficiency?

A
171
Q

What are the confirmatory testings done for adrenal insufficiency?

A
172
Q

What imaging is done for adrenal insufficiency?

A

 CT adrenals
* Small non-calcified adrenals in autoimmune causes
* Enlarge calcified adrenal in tuberculosis, metastatic disease and hemorrhage
 MRI pituitary
* Evaluate for any anatomical abnormalities

173
Q

What is the treatment of acute and chronic adrenal insufficiency?

A
174
Q

In adrenal insufficiency what steroid cover indications is needed for in surgery/trauma?

A
175
Q

What are the types of hyperparathyroidism and causes?

A
176
Q

What is the associated condition with parathyroid disorder?

A
177
Q

What is the moa of PTH?

A
178
Q

What are the SS of hypercalcemia?

A
179
Q

What is the clinical manifestation of hyperparathyrodiism?

A
180
Q

What is the blood tests and results for hyperparathyroidism?

A
181
Q

What is the summary of biochemical profiles for hyperparathyroidism?

A
182
Q

What are the radiological tests for hyperparathyroidism (not all are routine)?

A
183
Q

What is the medical treatment for hyperparathyroidism?

A
184
Q

What are the indications and contraindications for surgical intervention of hyperparathyroidism?

A
185
Q

What are the surgical options for hyperparathyroidism if the indications are met?

A
186
Q

Q1: What are the most common causes of hypercalcemia?
Q2: What investigations would you perform in a patient presenting with hypercalcemia?

A

 2 Most common causes
* Hyperparathyroidism
* Hypercalcemia of malignancy (secretion of PTH-like peptide)
 Less common causes
* Excess intake of vitamin D or calcium
* Hyperthyroidism
* Familial hypocalciuric hypercalcemia
* TB
* Sarcoidosis

 Serum albumin, phosphate, PTH, alkaline phosphatase (ALP)
* ↑ PTH, ↑ Ca2+, ↓ PO4- suggests hyperparathyroidism
* ↓ PTH, ↑ Ca2+ suggests hypercalcemia of malignancy
 24-hour urinary Ca2+ excretion  RFT

187
Q

Apart from serum total Ca+, PTH what other test would you do for patient?

A

 Investigations are targeted at defining possible complications due to increase PTH levels and hypercalcemia
 24-hour urinary Ca2+ excretion
* Document degree of hypercalciuria
 RFT
 Abdominal X-ray and USG kidneys
* Detect stones in urinary tract
 Bone mineral density (BMD) assessment
* At the forearm, hip and spine
* Assess degree of bone loss

188
Q

What is the bone involvement in hyperparathyroidism?

A
189
Q

What investigations can be done to help localize the abnormal parathyroid gland (hyperparathyroidism)?

A

 Radiological investigations to localize hyperactive or abnormal parathyroid gland
* Ultrasound (USG) (Can be intra-operative)
* CT scan
* MRI
* Radioisotope (Thallium,/ Sestamibi) scanning

190
Q

What are the indications for surgery in patients with primary hyperparathyroidism?

A

 Age < 50 years old
 Serum total Ca2+: 1 mg/dL above upper limit of normal
 24-hour urinary Ca2+ excretion (Hypercalciuria) > 200 mg  Creatinine clearance ↓ by ≥ 30 %
 Renal stones
 Osteoporosis

191
Q

What are the general features of subacute thyroidits?
What RF

A

 Self-inflammatory disease of the thyroid gland characterized by neck pain or discomfort, tender
diffuse goitre and a predictable course of thyroid function evaluation
* Also known as painful thyroiditis, subacute granulomatous thyroiditis and subacute non- suppurative thyroiditis
* MOST common cause of painful thyroid disease accounting for up to 5% of adult thyroid disease

 Family history of subacute thyroiditis
* Strongly associated with HLA-B35 or HLA-B67
* Results from a subclinical viral infection that provides an antigen that uniquely binds to HLA-B35 molecules on macrophages
* Resulting HLA-B35 complex activates cytotoxic T lymphocytes that damage thyroid follicular cells because the cells have partial structural similarity with the infection- related antigen

192
Q

What is the ddx for subacute thyroiditis?

A
193
Q

What is the clinical course of subacute thyroiditis?

A
194
Q

What is SS of subacute thyroiditis?

A
195
Q

What are the Ix for subacute thyroidits?

A
196
Q

What is the treatment for subacute thyroiditis?

A
197
Q

Where does phaeochromocytoma arise from
What is the classification of adrenal tumors?

A

 Arise from chromaffin cells of adrenal medulla and sympathetic ganglia
 Neuroendocrine tumour with serious and potentially lethal cardiovascular complications due to effects of secreted catecholamines

198
Q

Causes of phaeochromocytoma?

A
199
Q

What is the pathophysio of phaeochromocytoma?

A
200
Q

What is the arterial supply and venous drainage of arenal glands?

A

 Arterial supply
* Superior adrenal artery (from inferior phrenic artery)
* Middle adrenal artery (from aorta)
* Inferior adrenal artery (from renal artery)
 Venous drainage
* Left adrenal vein (drains into left renal vein)
* Right adrenal vein (drains into IVC directly)

201
Q

What is the classical triad of phaeochromocytoma and other signs?

A

 Classical triad (Tachycardia + Generalized sweating + Headache)
 5Ps of Phaeochromocytoma
* Pressure (BP: Sustained or paroxysmal hypertension)
* Pallor
* Palpitations (Tachycardia)
* Perspiration (Generalized sweating)
* Pain (Headache/ Chest pain)
 Other symptoms
* Dyspnea
* Tremor
* Generalized weakness
* Weight loss (hypermetabolism)
* Glucose intolerance

202
Q

What biochemical tests and imaging done to confirm dx and locate phaeochromocytoma?

A
203
Q

How to manage phaeochromocytoma
What are the preop preparations?
What complications?

A
204
Q

What are the 3 periodic paralysis disorders?

A
  • Thyrotoxic periodic paralysis
  • Hypokalemic periodic paralysis
  • Hyperkalemic periodic paralysis
205
Q

Thyrotoxic periodic paralysis

Age of onset
What is the etiology of thyrotoxicosis
What is precipitating factors
What is pathogenesis
Clinical features?
Attack frequency
Attack duration
Attack period
Biochemical features
Radiological features
Acute treatment
prevention

A

Over 20 years (20-39 years old)
Etiology: thyrotoxicosis (any etiology) –> graves disease is the most common cause
Precipitating factors: increased adrenaline and insulin release which shifts K+ into cells: stress, heavy excercise, high carbohydrate meals
Pathogenesis: thyroid hormone increases NaK+ ATPase activity which drives K+ into cells –> leads ot hyperpolarization of muscle membrane and relative inexcitability of muscle fibers
Clinical features: generalized weakness of sudden onset with preserved consiousness: proximal >distal and LL >UL, hypotonia, hyporeflexia, tachycardia, severe arrhythmia (sinus arrest/secondary AV block/VF/VT)
Attack frequency: infrequent (interval of weeks to months)
Attack period: usually at night or early in the morning, seasonal variation with more frequent attacks in summer months
Biochemical features: increased T3 and T4 level, decreased TSH level, increased CK level (rhabdomyolysis), hypoP, HypoMg
ECG findings (hypokalemia): sinus tachycardia, ST depression, prolonged QT interval, flattened T wave, presence of U wave, arrhythmia (sinus arrest/ 2nd AV block/VF/VT)
K+ during attack: low
Acute treatment: K+ supplementation: oral/IV KCl (aware of post treatment rebound hyperK when K+ moves back out of the cells
Prevention: IV propranolol (indicated in patients refractory to K+ adminstration). lifestyle modification: low carb diet, refrain from vigorous excercise

206
Q

Hypokalemic periodic paralysis

Age of onset
What is the etiology of thyrotoxicosis
What is precipitating factors
What is pathogenesis
Clinical features?
Attack frequency
Attack duration
Attack period
Biochemical features
Radiological features
Acute treatment
prevention

A

Age of onset: 10-20 years old
Etiology: hereditary hypokalemic PP (autosomal dominant)
Precipitating factors: increased adrenaline and insulin release which shifts K+ into cells: stress, heavy excercise, high carb meals
Pathogenesis: mutation in gene that codes for alpha1 subunit of Ca2+ channel in skeletal muscles: episodic K+ movement into cells causing weakness. Mutation in gene that codes for Na+ channel (SCN4A): anomolous gating pore current that causes aberrant depolarization during attacks of weakness
Clinical features: generalized weakness of sudden onset with preserved consiousness: Proximal > Distal and LL > UL  Progressive proximal myopathy, Later onset myopathy, Eventually develops in majority of patients after age 50 as paralytic attacks subsides, Hyporeflexia/ Areflexia
Attack frequency: infrequent (interval of weeks to months)
Attack duration: longer (hours-days)
Biochemical features: HypoK (during attack but normalize between attacks to distinguish it from secondary hypoK causes), genetic testing, provovative tests: excercise, ACTH administration
ECG (hypoK): ST depression, Prolonged QT interval, Flattened T wave, Presence of U wave, Arrhythmia (AF/ SVT/ VF). EMG: decreased amplitude of CMAP during attack
K+ during attack: low (K+ level normalized between attacks except secondary hypoK)
Acute treatment: K+ supplementation –> Oral/ IV KCl (aware of post-treatment rebound hyperkalemia when K+ moves back out of the cells)
Prevention: K+-sparing diuretics –>Spironolactone, Carbonic anhydrase inhibitors –> Acetazolamide/Dichlorphenamide
 Lifestyle modification: Low-carbohydrate diet, Refrain from vigorous exercise

207
Q

Age of onset
What is the etiology of thyrotoxicosis
What is precipitating factors
What is pathogenesis
Clinical features?
Attack frequency
Attack duration
Attack period
Biochemical features
Radiological features
Acute treatment
prevention

A

Age of onset: 1-10 years old
Etiology: hereditary hyperK PP (autosomal dominant)
Precipitating factors: stress, heavy excercise, fasting, K+ rich meals
Pathogenesis: mutation in gene that codes for Na+ channel (SCN4A): Na+ channel closes too slowly during resting phase, Na+ continues to leak into the muscle cells, leads to oversensitivity and stiffness in the muscels (myotoma)
Clinical features: generalized weakness of sudden onset with preserved consiousness, progressive proximal myopathy (later onset myopathy), eventually deveops in majority of patients after age 50 as paralytic attacks subside. Hypotonia, myotoma (delayed muscle contraction after contraction)
Attack frequency: frequent
Attack duration: shorter (mins-hours)
Biochemical features: increased K+ level, increased CK level, genetic testing, provocative tests: excercise, ACTH admin
ECG fingins: peaked T wave (hyperK). EMG: electrical myotoma
K+ during attack: high/normal
Acute treatment: thiazide diuretics (hydrochlorothiaizide), inhaled B2 agonists: albuterol, stimulates Na+ K+ pump which increases K+transport into cells (most attacks to not require treatment as they are brief
Prevenetion: Thiazide diuretics =Hydrochlorothiazide, Inhaled β2-agonist * Albuterol, Carbonic anhydrase inhibitors * Acetazolamide * Dichlorphenamide
 Lifestyle modification: Low-carbohydrate diet, Refrain from vigorous exercise

208
Q

What is the ddx of generalized weakness?

A

 Myasthenia gravis (MG)
 Botulism
 Guillain-Barre syndrome (GBS)
 Transverse myelitis
 Secondary hypokalemic PP
* Thyrotoxic periodic paralysis
* Hyperaldosteronism
* Renal tubular acidosis
o Type I: Distal RTA
o Type II: Proximal RTA

209
Q

What are the RF for thyroid cancer?

A
210
Q

What are the types of thyroid cancer?

A
211
Q

What is the physiological effects of thyroid hormones?

A
212
Q

What is the tumor characteristics of papillary, follicular, medullary, anaplastic thyroid cancer
RF, clinical course, mode of spread, distant spread, cytological features, prognosis

A
213
Q

What is TNM staging of thyroid cancer?

A
214
Q

What is SS of thyroid cancer
Local extension
metastasis

A
215
Q

What is done in general exam for suspected thyroid cancer?

A
216
Q

What is done for inspection in suspected thyroid cancer?

A
217
Q

What is done for palpation, percussion and auscultation for thyroid cancer?

A
218
Q

What blood tests done for thyroid cancer?

A
219
Q

What is is 1st line imaging for thyroid mass
What findings are suspicious for throid cancer?

A
220
Q

What is the sonographic criteria for FNA in thyroid mass?
Patterns that increase chance of malignancy

A
221
Q

What is the indications for FNAC in thyroid mass
What classification system for cytology results?

A
222
Q

What is the use of assessing the functionality of the thyroid nodule?
How is it tested

A
223
Q

What imaging ix to find out extent and staging of thyroid cancer?

A
224
Q

What is treatment for papillary thyroid carcinoma?

A
225
Q

What is treatment for papillary thyroid carcinoma?

A
226
Q

What is treatment for medullary thyroid carcinoma?

A
227
Q

What is treatment for anaplastic thyroid carcinoma?

A
228
Q

What is preop prep for thyroid cancer?

A

 Anti-thyroid drugs or β-blockers
* Prevention of thyroid storm
 Calcium supplements and vitamin D
* Prevention of postoperative hypocalcemia
* Prevention of hungry bone syndrome (HBS)
 Lugol’s solution
* Block iodine uptake and secretion of thyroid hormone
* Decrease vascularity of thyroid gland to reduce intraoperative bleeding

229
Q

What are adv and disadv of total thyroidectomy vs hemithyroidectomy?

A
230
Q

What is the lymph node dissection options for thyroid cancer?

A
231
Q

What are the immediate, early and late complications of thyroidectomy?

A
232
Q

When is thyroid hormone replacement needed post thyroidectomy?

A
233
Q

What indications for radioactive iodine ablaton (I131) done in thyroid cancer
What is prep before RAI ablation
What is done after RAI ablation

A
234
Q

What is the post op management after thyroidectomy (thyroid cancer)?

A
235
Q

What is the risk stratification to predict disease specific mortality in thyroid cancer?
What prognostic factors?

A

MBBS VI Medicine (93 decks)

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