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Sandra Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What does your body have trouble moving if you have diabetes Mellitus? What is the result of this?

A

Has trouble moving glucose from the blood into cells

This results in high levels of glucose in your blood, and not enough of it in your cells results in energy depletion of cells.

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2
Q

What hormones control how much glucose is in the blood relative to how much gets into the cell

A

Insulin: reduce blood glucose levels
Glucagon: Increase blood glucose levels

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3
Q

Where are glucagon and insulin secreted from?

A

Islets of Langerhans within pancreas

Beta cells: insulin
Alpha cells: glucagon

REMEMBER Alpha = glucAgon

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4
Q

How does insulin reduce the amount of glucose in the blood

A

Binds to insulin receptors embedded in the cell membrane of various insulin-responsive tissues like adipose tissue and muscle cells

When activated, the insulin receptors cause vesicles containing glucose transporter within the cell to fuse with the cell membrane allowing glucose to be transported into the cell

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5
Q

How does glucagon increase the amount of glucose in the blood

A

Raises blood glucose levels by getting the liver to generate new molecules of glucose from other molecules and break down glycogen into glucose

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6
Q

What is diabetes mellitus

A

A group of chronic disorders characterised by abnormal glucose metabolism resulting in elevated glucose levels

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7
Q

Type 1 Diabetes vs Type 2 diabetes

A

Type 1 : Body doesnt produce insulin.Autoimmune destruction of beta cells in the pancreas
Type 2 : Makes insulin but the body doesnt respond to it. Insulin resistance followed by beta cell atrophy

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8
Q

Classification of Type 1 Diabetes Mellitus

A

Type 1 diabetes is B-cell destruction leading to absolute insulin deficiency. It accounts for 5-10% of all diabetes. Type I diabetes is divided into two types: Immune-mediated and idiopathic. The traditional paradigm is of childhood-onset with acute symptoms of DKA.

Type 1A: immune-mediated diabetes
-Most common
-Autoimmune destruction of pancreatic beta-cells -> decrease in insulin
-Type IV hypersensitivity response

Type 1B: idiopathic diabetes
-No evidence of autoimmunity
-Varying degrees of low insulin, episodes of ketoacidosis

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9
Q

Cause of Type 1 diabetes

A

Genetic abnormality causes a loss of self-tolerance among T cells that target beta-cell antigens. This means beta cells are attacked, and less insulin and glucose pile up in the blood because they can’t enter the body’s cells

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10
Q

What is latent autoimmune diabetes

A

A progressive form of autoimmune diabetes
Onset is at >30 years old

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11
Q

Risk factors of Type 1 diabetes

A

Genetic predisposition
Multiple gene polymorphisms associated with DM Type 1

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12
Q

Diagnosis of Type 1 diabetes mellitus

A

The age of onset and rate of B-cell destruction is quite variable:

  • Rapid in infants and children
  • Slow in others (mainly adults), such as in Latent AutoimmunenDiabetes of Adulthood (LADA).
    This influences clinical presentation and may confuse the diagnosis.

Diabetes:
Acute onset of hyperglycaemic symptoms with ketoacidosis:

  • Random plasma glucose > 11.1 mmol/L consistent with diagnosis
  • HbA1c is not used in diagnosis

Autoimmune markers are not routinely used but can include:

  • Glutamic acid decarboxylase (GAD65)
  • Insulin (IAA)
  • Tyrosine phosphatases (IA-2 & IA-2B)
  • ZnT8

Low or undetectable plasma C-peptide level supports the diagnosis.

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13
Q

Latent autoimmune diabetes of adulthood

A
  • A subtype of autoimmune Type 1 diabetes is sometimes misdiagnosed as T2D.
  • Slowly progressive destruction of Beta cells.
  • May appear to respond to oral agents initially.
  • Less likely to have other features of metabolic syndrome (central obesity, HT, dyslipidaemia).
  • More likely to have a history of other autoimmune diseases.
  • Starting insulin early may help to preserve beta cell insulin production

Criteria to standardize the definition:

  1. Age of onset usually > 30y
  2. Positive titre for at least one T1D autoantibody
  3. Not treated with insulin within the first 6 months after diagnosis
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14
Q

Complications of Type 1 diabetes

A
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15
Q

What are the sign and symptoms of Type 1 diabetes (8)

A
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16
Q

What are the management of Type 1 diabetes

A
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17
Q

What is diabetic ketoacidosis

A

A condition resulting from deficient insulin availability, leading to lipid oxidation and metabolism rather than glucose metabolism. The insulin absence results in free fatty acid (FFA) released from adipose tissue and in unregulated hepatic FFA oxidation and ketogenesis.

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18
Q

diabetic ketoacidosis characterised by?

A

severe hyperglycemia
accelerated ketogenesis.

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19
Q

What is a serious complication of Type 1 diabetes

A

Diabetic ketoacidosis (DKA)

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20
Q

Clinical Presentation of diabetes mellitus type 1

A

Signs of dehydration
* polyuria
* polydypsia
* weight loss
GI symptoms
Hyperventilation (↑Respiratory Rate - Kussmaul breathing)
True coma - 10% of cases)

Side Note Kussmaul breathing is air hunger, rapid deep breathing a sign of metabolic acidosis. This is different to Kusmaul’s sign looks at JVP relationship with breathing.

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21
Q

DKA Aetiology (5I’s) + Initial Diagnosis

A
  • Infection
  • Infarction
  • Insufficient insulin
  • Intercurrent illness
  • Inappropriate withdrawal of Insulin
  • Initial Diagnosis
    Remember Precipitating factors of DKA 5 I’s: Infection Ischemia Infarction Intoxication Insulin missed
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22
Q

Investigations of DKA

A
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23
Q

Complications of DKA

A

Cerebral oedema
* May be caused by very rapid reduction of blood glucose, use of hypotonic fluids and/or bicarbonate
* High mortality
* Treat with mannitol, oxygen
Acute respiratory distress syndrome
Thromboembolism
Disseminated intravascular coagulation (rare)
Acute circulatory failure

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24
Q

Differential diagnosis of DKA- high blood glucose and coma

A

Head injury
Alcohol
Drug overdose

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25
Q

Risk Factors of DKA

A

Infection
Stress
Irregular insulin use

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26
Q

Diagnosis of DKA

A

Diagnosis of DKA

Hyperglycemia (>11.1mmol/L)
Metabolic acidosis (pH <7.3 or <HCO3-)
* Severity is assessed this way
Hyperketonemia
Ketonuria

Side Effects Different types ketones produced include B-Hydroxymutyrate, acetatoacetate and acetone

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27
Q

Treatment for DKA

A
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28
Q

________ breathing presents as rapid, deep breathing and is seen in diabetic ketoacidosis

A

Kussmaul

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29
Q

What type of diabetes is more commonly associated with diabetic ketoacidosis?

A

Type 1 DM

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30
Q

What compound that gives patients with diabetic ketoacidosis a fruity odor to their breath

A

Acetone

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31
Q

In diabetic ketoacidosis, total body stores of potassium are (high/low)

A

Low

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32
Q

Diabetic ketoacidosis causes increased production of ketones such as

A

beta-hydroxybutyrate and acetoacetate.

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33
Q

Diabetic ketoacidosis causes a(n) (increase/decrease) _______ in epinephrine production

A

increase

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34
Q

Diabetes mellitus type (1/2) __ is caused by a type IV hypersensitivity reaction

A

1

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35
Q

The primary defect in diabetes mellitus type 1 is autoimmune destruction of the ____ of the pancreas

A

Beta cells

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36
Q

Type 1 diabetes is usually diagnosed (before/after) ___ the age of 30

A

Before

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37
Q

What is the primary defect of diabetes mellitus type 2

A

Increased insulin resistance

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38
Q

Risk Factors of type 2 diabetes

A
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39
Q

Signs and symptoms type II diabetes

A

Asymptomatic period
Infections
Fatigue
Blurred vision
4Ps
* Paresthesia
* Polydipsia
* Polyuria
* Polyphagia

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40
Q

Causes of Type 2 diabetes

A
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41
Q

Patients with diabetes mellitus type 2 have (high/low) __ insulin sensitivity

A

low

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42
Q

Risk Factors of DKA

A

Multifactorial; interaction between genetic, environmental, behavioural factors

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43
Q

Why is diabetes ketoacidosis rare in DM type 2?

A

As endogenous insulin prevents lipolysis

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44
Q

Diabetic Complications (advanced disease)

A

**Diabetic Retinopathy

Poor vision

Diabetic Neuropathy
Peripheral neuropathy
* pain
* loss of sensation
* dysaesthesia
* weakness
Autonomic neuropathy
* resting tachycardia
* orthostatic hypotension
* erectile dysfunction
* constipation

Diabetic Nephropathy

Oedema
Anaemia
Hypertension
Uremia

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45
Q

What is the most common intial manifestation of type 2 DM

A

elevated blood glucose with ketonemia.

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46
Q

What is the best pharmocological treatment for type 2 DM

A

Metformin

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47
Q

NICE provide guidelines on how drug therapy should be used in T2DM:

A
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48
Q

Table comparing T2DM medications

A
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49
Q

Investigations of Type 2 diabetes

A
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50
Q

Differential Diagnosis of Type 2 diabetes

A
Other diagnostics include Physical examination : Fundoscopic exam: cotton wool spots, flare haemorrhages Monofilament testing: decrease in sensation Lower extremities: decrease in pedal pulses, presence of ulcers
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51
Q

How to differentiate Type 2 diabetes from Type 1

A

Type 2 diabetes differs from Type 1 in the following ways:
doesnt have autoantibodies
C peptide : normal/ elevated

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52
Q

Aetiology of type 2 diabetes

A

Genetic predisposition
Physical inactivity and being overweight contributes to insulin resistance.

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53
Q

Management of Type 2 diabetes

A

Management

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54
Q

Pharmacology for diabtes mellitus type II

A

Indications for Insulin
Acute metabolic complications
Perioperative in patients undergoing surgery
Severe infection
Pregnancy and lactation
Fasting plasma glucose >300mg/d
Failure of oral anti-diabetic agent/contraindication of oral anti-diabetic agents

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55
Q

Screening for Diabetic Complications

A
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56
Q

For which type of diabetes is Hyperosmolar Hyperglycaemic state more likely to occur?

A

Type 2

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57
Q

Complications and prognosis for diabetes mellitus type II

A
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58
Q

Type I vs Type II Diabetes

A
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59
Q

Hyperosmolar Hyperglyaecmic State

A

is a complication of type 2 diabetes. It involves extremely high blood sugar (glucose) levels without the presence of ketones.

Hyperosmolar Hyperglycaemia (HOH) state occurring primarily in type 2 diabetes and is characterised by marked hyperglycaemia and dehydration without ketoacidosis. The disturbance in consciousness in patients varies from drowsy to comatose. HOH is a more sinister complication than ketoacidosis with a mortality rate as high as 50%.

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60
Q

What does a hyperosmolar hyperglycemic state cause

A

increased plasma osmolarity due to extreme dehydration and concentration of the blood

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61
Q

Diagnosis of hyperglycaemic state

A
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62
Q

Pathophysiology hyperglycaemic state

A

This condition results from a combination of insulin deficiency and counterregulatory hormone excess. The insulin present stops ketone production but in insufficient quantities to prevent worsening hyperglycemia.

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63
Q

Management of hyperglycaemic state

A
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64
Q

complication of hyperglycaemic state

A

Venous thromboembolism

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65
Q

Hypoglycaemia

A
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66
Q

What is hyperthyroidism

A

denote conditions in which hyperfunction of the thyroid leads to thyrotoxicosis.

The most common cause of hyperthyroidism are Graves disease, multinodular goitre, an autonomously functioning thyroid nodule (adenoma) and subacute thyroiditis. Graves Disease is more common in women. Multinodular goitre is more common in the elderly. Graves disease typically manifests in middle aged women. Thyroid diseases are more common in women.

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67
Q

What is the hypothalamic-pituitary-thyroid axis

A

TRH (thyroid-releasing Hormone) stimulates the synthesis and secretion of TSH (thyroid-stimulating hormone)

TSH acts at the thyroid to stimulate all steps of thyroid hormone (T3 + T4) bio synthesis and secretion by binding onto TSH receptors

T3 + T4 inhibit TSH + TRH via negative feedback system

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68
Q

What does it mean for the hypothalamic-pituitary-thyroid axis with an individual diagnosed with hyperthyroidism

A

Elevated circulating T3 + T4
Since there is a negative feedback loop with TRH and TSH it means that there will be a decrease in those hormones

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69
Q

How are T3 and T4 (thyroid hormone) synthesised

A

1.TRH release from paraventricular nucleus from hypothalamus
2.Anterior pituitary to release from TSH
3.TSH stimulates follicle cells of the thyroid to synthesise thyroglobulin
4.Iodide trapping
5.Oxidation of iodide via thyroid peroxidase
6.Iodination of tyrosine amino acids
7.Couple of the DIT + MIT
8.Endocytosis of thyroglobulin with T3 + T4
9.Lysosomal enzymes cleave T3 + T4 out of thyroglobulin
10.Exocytosis of T3 + T4 into blood plasma

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70
Q

What does the Thyroid hormone do?

A

Promotes normal bone growth + maturation

Promotes muscular function and development

Increase basal metabolic rate/ O2 usage

Promotes normal C.O

Promotes an increase in synapses/myelinations/dendrites

Promotes G.I motility + secretions

Promotes normal hydration of skin

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71
Q

How is T3 + T4 made from tyrosine molecule

A

Tyrosine is broken down into T3 + T4 components via lysozyme enzymes

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72
Q

What makes up the thyroid hormone?

A

T4 thyroxine +

T3 triiodothyronine

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73
Q

What does thyroid peroxidase do?

A

Iodide oxidation: turns iodide ions into iodine

Iodination: puts I2 onto amino acids on tyrosine amino acids

Fuses DIT + DIT = T4 (Throxine)

Fuses MIT + DIT = triodothyronin

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74
Q

How does iodide enter from the blood into follicles of the thyroid gland

A

secondary active transport

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75
Q

Causes of hyperthyroidism

A

Graves disease: Most common
Toxic multinodular goitre: multinodular hyperplasia, <50% are thyrotoxic
Toxic adenomas: benign, solitary, discrete encapsulated nodules, usually non-toxic but can cause mild hyperthyroidism

Other causes: thyroiditis, carcinoma, TSH-secreting pituitary tumour, iatrogenic (iodine T4), choriocarcinoma, hydatidiform mole (rare)

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76
Q

Investigations to identify hyperthyroidism

A

TSH, free T3 & T4, Full Blood count, liver enzymes and erythrocyte sedimentation rate (ESR)
Thyroid antibodies (antithyroid peroxidase [TPO] or TSH-R antibodies)
Isotope scan (I123)

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77
Q

Clinical Presentation of hyperthyroidism

A

Hyperactivity, irritability, altered mood, insomnia
Heat intolerance, sweating
Palpitations
Fatigue, weakness
Dyspnea
Weight loss with increased appetite (weight gain in 10% of patients)
Pruritus
Increased stool frequency
Thirst and polyuria
Oligomenorrhea or amenorrhea; loss of libido

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78
Q

Clinical examination of hyperthyroidism

A

General: irritability, axious, weight loss, warm, moist skin, chorea, periodic paralysis (primarily in Asian males), psychosis (rare)
Hands: onycholysis, fine tremor
Face: Hair loss, Graves opthalmology
Cardiovascular: Sinus tachycardia, atrial fibrillation, palmar erythema, congestive (high-output) heart failure,
Neurological: hyperkinesia, hyperreflexia, muscle weakness and wasting
Legs: pretibial myxoedema

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79
Q

Features of Severe Hyperthyroidism

A

Atrial fibrillation
Heart Failure
Significant weight loss
Proximal myopathy

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80
Q

Graves Disease Additional Manifestation

A

Diffuse goiter
Ophthalmopathy
Localised dermopathy
lymphoid hyperplasia
Thyroid acropachy

81
Q

Differential dioagnosis of hyperthyroidism

A
82
Q

Investigations for hyperthyrodism

A
83
Q

Causes of hyperthyroidism

A
84
Q

Pathology of hyperthyroidism

A
85
Q

Pathophysiology of hyperthyroidism

A
86
Q

What treatment is given for indivualds with hyperthyroidism

A

Beta blockers: to treat immediate symptoms

Anti-thyroid drugs: block thyroid hormone production + release

Radioiodine therapy: partially or completely destroy thyroid function followed by replacement thyroid therapy

87
Q

Complications of hyperthyroidism

A

Complications
Complications of thyroidectomy
Recurrent laryngeal nerve damage
Hypoparathyroidism
Thyroid crisis
Local hemorrhage, causing laryngeal edema
Wound infection
Hypothyroidism
Keloid formation

88
Q

Thyroid storm

A
89
Q

What is multinodular goitre

A

defined as an enlarged thyroid with multiple nodules that yields a hyperthyroid state.

90
Q

Subacute granulomatous DeQuervain thyroiditis what is it?

A

type of thyroiditis that presents as a tender thyroid with transient episodes of hyperthyroidism.

91
Q

What is Graves disease

A

Autoimmune disorder of the thyroid gland that causes hyperthyroidism

92
Q

A characteristic sign of Graves’ disease includes

A

pretibial myxedema

due to activation of dermal fibroblasts that express the thyroid stimulating hormone receptor.

93
Q

Thyroid stimulating hormone levels are (increased/decreased) ___ in Graves’ disease

A

decreased

94
Q

What is a fatal complication of graves disease

A

thyroid storm

95
Q

What is hypothyroidism

A

Variety of abnormalities that cause insufficient secretion of thyroid hormones. The most common cause is autoimmune thyroid disease
Primary hypothyroidism is decreased production of thyroid hormones because of thyroid gland disease (most common is hashimoto’s thyroiditis). Secondary hypothyroidism is a problem in the Pituitary gland or hypothalamus resulting in ↓TSH leading to ↓Thyroid hormone production.

96
Q

Primary causes of hypothyroidism

A

-Autoimmune:
Hashimoto’s thyroiditis is characterised by lymphocytic infiltration of the gland and progressive destruction of functional thyroid tissue (goitre)
Primary atrophic hypothyroidism (no goitre)

-Other causes
Post-total or partial thyroidectomy or radioiodine treatment
Drug-induced with TSH receptor-blocking antibodies
Subacute thyroiditis (de Quervain’s): after the hyperthyroid phase
Postpartum thyroiditis
Congenital (rare)

97
Q

Secondary causes of hypothyroidism

A

Secondary to pituitary failure (reduced TSH production)
Iodine deficiency (commonest cause worldwide)

98
Q

Risk factors for hypothyroidism

A

Iodine deficiency
Female sex
Middle age
Family History
Autoimmune disorders
Graves’ disease
Post-partum thyroiditis
Turner’s and Down’s syndromes
Primary pulmonary HTN
Multiple sclerosis
Radiotherapy
Iodine deficiency
Amiodarone use and lithium use

99
Q

Signs and symtpms of hypothyroidism

A
100
Q

Differential diagnosis for hypothyroidism

A

Primary Hypothyroidism has many causes - identify the cause with investigations
Secondary Hypothyroidism
Pituitary adenoma
Malignancy of the hypothalamus
Depresssion
Alzhiemer’s Dementia
Anaemia

101
Q

Investigations for hypothyrioidism

A
102
Q

Treatment for hypothyroidism

A

Mainstay of treatment is oral thyroxine; aim to restore TSH to normal with dose titrated according to age, gender and clinical status

103
Q

Complications and porgnosis of hypothyroidism

A
104
Q

Myoxedema coma

A

Myoxedema coma is a serious emergency, due to severe untreated hypothyroidism, and typically presents with impaired consciousness, hypoventilation and hypothermia. Hospitalizations is essential for initial treatment.

105
Q

Hashimoto thyroiditis presents with an increased risk for

A

primary B-cell lymphoma.

106
Q

What is Hashimoto thyroiditis

A

autoimmune cause of hypothyroidism that presents with a moderately enlarged, nontender thyroid.

107
Q

How does amiodarone affect thyroid?

A

Amiodarone induces alterations in thyroid hormone levels by actions on thyroidal secretion, on the peripheral tissues, and on the pituitary gland.

These actions result in elevations in serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations.

108
Q

Complications of hyper/hypo thyroidism

A

Hyperthyroidism: thyroid storm
Hypothyroidism: myxedema, cretinism (infants, young children)

109
Q

Types of thyroid cancers

A

-Papillary thyroid: most common, least agressive
-Follicular thyroid: 2nd most common
-Medullary thyroid carcinoma
-Anaplastic/undifferentiated carcinoma

110
Q

Causes of thyroid cancer

A

Irradiation
Iodine - follicular carcinoma
Genetic syndrome (RET/PTC1, RET/PTC2 and RET/PTC3 TRK (less common)
Papillary microcarcinoma of the thyroid (PMC)

111
Q

Risk factors of thyroid cancers

A
112
Q

Signs and synptoms of thyroid cancers

A
113
Q

Diagnosis of thyroid cancer

A
114
Q

Treatment for thyroid cancer

A

Surgery
Thyroglobulin is the marker to measure thyroid cancer function post treatment

115
Q

What is pituitary adenoma

A

Benign anterior pituitary tumour arising from specific cell types

116
Q

Signs and symptoms of pituitary adenoma

A

Adjacent structure compression
-Visual changes (e.g diplopia, bitemporal hemianopsia), headache

117
Q

Conditions which may be caused by pituitary adenoma

A

Cushing disease
Acromegaly
Prolactinoma

118
Q

What are potential complications of pituitary adenoma if there is compression of the central satiety center of the hypothalamus

A

Hyperphagia and weight gain

119
Q

What is a potential complications of pituitary adenoma if the oculomotor nerve (cranial nerve III) is compressed.

A

Oculomotor palsy

120
Q

What is the most common pituitary adenoma

A

Prolactinoma

121
Q

pituitary adenoma

A
122
Q

What is Cushing disease defined as

A

ACTH-dependent syndrome is characterised by excess corticosteroid production from the adrenal glands. It is ACTH-dependent because an ACTH-secreting pituitary tumour triggers it. Cushing’s syndrome is an overarching term to describe hypercortisolemia dependent of independent of ACTH. Adrenal Cushing’s syndrome is different because it is hypercortisolemia independent of ACTH.

Is hypercortisolemia from an ACTH-secreting pituitary tumour (ACTH Dependent)

123
Q

Cushing’s syndrome (CS)

A

Cushing’s syndrome (CS): is a disease complex that results from chronic hypercortisolemia of any cause. The causes may be classified as ACTH dependent and ACTH independent.

124
Q

Serum adrenocorticotropic hormone levels are (increased/decreased) ____ in adrenocorticotropic hormone independent Cushing syndrome

A

decreased

125
Q

Serum adrenocorticotropic hormone levels are (increased/decreased) _____ in adrenocorticotropic hormone dependent Cushing syndrome.

A

increased

126
Q

Clinical features that best distinguish Cushing’s syndrome

A

Clinical features that best distinguish Cushing’s syndrome: Facial appearance: moon face and plethoric complexion, ecchymoses, Violaceous striae on abdomen, thighs and axillae, Proximal muscle weakness. In children, weight gain with decreased growth velocity. Early bone fractures, especially atraumatic rib or vertebral fractures

127
Q

Differential Diagnosis and causes of Cushing’s syndrome

A
128
Q

Investigations of cushing disease

A
129
Q

Causes of cushings disease

A

The majority of endogenous Cushing’s syndrome is due to ACTH-secreting pituitary adenomas (Cushing’s disease).

Remember Cushing’s Disease is ACTH dependent hypercortisolaemia. Most common cause is pituitary adenoma

130
Q

Diagnosis of Cushings disease

A

Overnight dexamethasone suppression test (first line test)
-False positives (pseudo Cushing’s) seen in depression, obesity, alcohol excess and inducers of liver enzymes (e.g phenytoin, rifampicin)

24-hour urinary free cortisol
48-hour dexamethasone suppression test

131
Q

Management of cushings disease

A
132
Q

Complications of cushings disease

A
133
Q

Adrenal Insufficiency

A
134
Q

How is acromegaly caused?

A

From hyposecretion of gonadotropin

Due to pituitary adenoma in 90% of cases. May also be from non-pituitary tumours of the pancreas, lungs and adrenal glands secondary to gonadotropin-releasing hormone (GnRH) secretion

135
Q

Other complications of acromegaly

A

Diabetes
Congestive cardiac failure
Renal failure
Oligomenorrohoea/amenorrhoea
Impotence/erectile dysfunction
Obstructive sleep apnea

136
Q

What is the cause of a prolactinoma

A

Benign lactotroph cell tumour in anterior pitiutary -> prolactin (PL) secretion, prolactinemia

137
Q

What is Conn’ s syndrome

A

also known as primary hyperaldosteronism, refers to the excessive secretion of the hormone aldosterone despite normal renin levels

138
Q

Definiton and aetiology of Addisons disease

A

Primary adrenocortical deficiency results from destruction of the adrenal cortex, adrenal dysgenesis or impaired steroid genesis

-Glucocorticoid, mineralocorticoid and sex steroid levels are reduced

139
Q

Causes of primary Addisons disease (hypoadrenalism)

A

Autoimmune adrenalitis (80%), TB, metastasis, HIV, amyloidosis, fungal infiltration, haemochromatosis, adrenoleucodystrophy, Waterhouse-Freiderichson syndrome

140
Q

What is syndrome of inappropriate antidiuretic hormone secretion (SIADH)

A
141
Q

Causes of SIADH

A
Also medications and surgery/injury to pituitary are causes of SIADH
142
Q

Signs and symptoms of SIADH

A
143
Q

What is diabetes insipidus

A

Disorder resulting from deficiency of ADH or its action

Diabetes Insipidus (DI) is associated with inadequate arginine vasopressin (known as antidiuretic hormone) secretion or renal response to arginine vasopressin, resulting in hypotonic polyuria and a compensatory/underlying polydipsia. There are two main types of diabetes insipidus, central DI and nephrogenic DI

Triad Polyuria, dilute urine, and increased thirst are characteristic of DI

144
Q

Pathophysiology of diabetes insipidus

A

Antidiuretic hormone is initially produced by the hypothalamus and then transported to the posterior pituitary gland via the pituitary stalk for storage.

When osmoreceptors sense hyperosmolarity in the blood it stimulates the posterior pituitary gland to release ADH into systemic circulation.

ADH acts on the kidneys and activates the arginine vasopressin 2 (AVP2) receptors of the renal collecting duct which increases the generation of aquaporin 2. Aquaporin 2 channels increases water retention

As a result, there is a net increase in water reabsorption in the collecting duct, leading to appropriate reservation of water and concentrating urine.

Think To little ADH or lack of response of the kidney to ADH means less water retention and more water output resulting in polyuria

145
Q

Risk Factors of DI

A
146
Q

Signs and symptoms of DI

A
147
Q

Differential diagnosis of diabetes insipidus

A

Diabetes Mellitus Type I
Diabetes Mellitus Type II
Benign prostate hyperplasia
Excessive fluid intake
Pituitary adenoma
Craniopharyngioma
Psychogenic polydipsia
Hyperaldosteronism
Medications (Diuretics overdose)
Hypercalcaemia
Hyperosmolar hyperglycaemic state (HHS)
Urinary tract obstructions (prostatic hypertrophy, osmotic diuresis)

148
Q

Investigations DI

A
149
Q

Aetiology DI

A

Central DI (also known as neurogenic DI) caused by insufficient synthesis or release of ADH from the central nervous system

Nephrogenic DI caused by ineffective response to ADH in the kidneys, such as defective ADH receptors caused by genetic defects.

Dipsogenic DI (also known as primary polydipsia) results from excessive fluid intake practiced over an extended period. Sometimes not classified as a true diabetes insipidus.

Gestational DI During pregnancy, vasopressins are more readily metabolised peripherally by placenta hormones. Hence it can provoke transient “central DI” in some patients. Commonly, this condition resolves spontaneously upon delivery.

150
Q

Pathophysiology of DI

A

Central Diabetes Insipidus

Traumatic or pathological damages affecting the hypothalamus or posterior pituitary gland causes cell death in hormone secreting cells in those areas, thus affecting the normal secretion and release of ADH. Without appropriate stimulation of ADH in the kidneys, renal collecting ducts lost its ability to perform adequate water reabsorption essential for volume maintenance of the body, resulting in a diuretic phenomenon.

Nephrogenic Diabetes Insipidus

Nephrogenic DI is caused by defective ADH receptors in the kidneys. Normally, two receptors AVPR1 and AVPR2 responds to increasing levels of ADH in the systemic circulation. AVPR1 is responsible for vasoconstriction and prostaglandin release, whereas the AVPR2 receptors mediated the antidiuretic response as well as certain coagulation factors (factor VIII and von Willebrand’s factor), hence unresponsive AVPR2 receptors in nephrogenic DI causes diuretic effects as well as mild coagulation defects.

151
Q

Management of DI

A
152
Q

Complications of DI

A

Hypernaturaemia
Growth retardation
Hydronephrosis

153
Q

What is hyperparathyroidism

A
154
Q

What are the types of hyperparathyroidism

A

Primary
Secondary
Tertiary

155
Q

Differential diagnosis of hyperparathyroidism

A
156
Q

Investigations for hyperparathyroidism

A
  • PTH
  • FBC
  • EUC
  • Vitamin D
  • LFTs
  • Thyroid Function test
  • Urinary calcium
  • Multiple Myeloma screening?
    Once you have confirmed hyperparathyroidism (i.e. high PTH, high calcium, high urine calcium , low or normal phosphate, high ALP, more likely to be chronic, long standing, hypercalcaemia) then you can consider imaging:
  • Bone Mineral Density Scan (DEXA) in primary hyperparathyroidism - Osteoporosis, osteopenia
  • Renal imaging (abdo x-ray or U/S) - Nephrocalcinosis
157
Q

causes of hyperparathyroidism

A

Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, leading to hypercalcaemia. Causes:

  • Parathyroid adenomas (85%)
    MEN 1 and MEN 2 (15%)
    Malignancy (<1%)
  • External neck irradiation. Lithium therapy, often used to treat patients with bipolar disorder, can lead to the over-stimulation of parathyroid glands (rare)

Multiple Endocrine Neoplasia (MEN) are a group of familial endocrine diseases that affect multiple endocrine glands. There are two main types: MEN-1 and MEN-2.

158
Q

Risk factors of hyperparathyroidism

A

Genetic mutations
-Multiple endocrine neoplasia (MEN) syndrome

159
Q

complications for hyperparathyroidism

A

Post Surgery
* Haematoma
* Hypocalcaemia
* Larygneal nerve injury
* Pneumothorax
Osteoporosis
Bone Fractures
Nephrolithiasis

160
Q

Signs and symptoms of hyperparathyroidism

A
161
Q

Treatment for hyperparathyroidism

A
162
Q

Pathology and causes of hypoparathyroidism

A
163
Q

Causes of hypoparathyroidism

A
164
Q

Signs and symptoms of hypoparathyroidism

A
165
Q

What are the treatment for hypoparathyroidism

A
166
Q

What is hypercalcemia?

A

Higher than normal calcium levels in the blood (over 10.5mg/dL)

One of the most common biochemical abnormalities in the body is elevated calcium levels in the blood, which is referred to as hypercalcaemia . Primary hyperparathyroidism and malignancy are the two most common causes of increased serum calcium levels. The presence of high or not adequately suppressed serum parathyroid hormone levels should point the diagnosis towards hypercalcaemia of parathyroid origins. Severe hypercalcaemia requires admission to hospital and treatment with aggressive intravenous hydration and bisphosphonates along with treatment of the underlying disease

167
Q

Clinical Presentation of hypercalcaemia

A

“Bones, stones, thrones groans, moans”

Stones: nephrolithiasis
Bones: bone pain, myalgia, muscle cramps
Thrones: constipation, polyuria
Abdominal Groans: abdominal pain
Psychiatric Moans: anxiety, depression, memory loss, unsteady gait, poor sleep, parasthesia

168
Q

What causes hypercalcaemia?

A

CHIMPS

C-Cancer
H-Hyperparathyroidism
I-Intoxication of vitamin D/Idiopathic
M-Milk alkali syndrome/Multiple myeloma
P-Paget’s disease
S-Sarcoidosis

169
Q

Calcium regulation

A

Calcium regulation is primarily controlled by the parathyroid hormone produced by the parathyroid gland. The parathyroid glands are tan-coloured, bean-shaped structures, about the size of a grain of rice. There are 4 parathyroid gland which lie on the posterior surface of the thyroid gland. Parathyroid gland main purpose is to synthesise and secrete parathyroid hormone (PTH). The parathyroid hormone does this in response to blood calcium levels.

  • ↓Serum Ca2+ → Stimulates Parathyroidgland → Chief cells secrete PTH → ↑PTH aims to ↑Serum Ca2+

The normal range of serum calcium is 2.25-2.65mmol/L

Calcium is transported in blood bound to albumin. Some travel as free serum calcium.

170
Q

Timing and Severity of hypercalcaemia.

A
  • Sudden = more likely malignancy
  • Chronic = more likely hyperparathyroidism
  • > 3.7 really high = malignancy (parathyroid)
171
Q

Differential Diagnosis of Hypercalcaemia

A
  • Hyperparathyroidism
  • Malignancy
  • PTH-like peptide
  • Bone metastasis
  • Sarcoidosis
  • Dehydration and Prolonged immobilisation
  • Hyperthyroidism
  • Familial hypocalciuric hypercalcaemia
  • Drugs

Remember 90% of hypercalcaemia cases are cause by primary hyperparathyroidism or by malignancy

172
Q

Approach to patient with hypercalcaemia (>2.65mmol/L)

A
173
Q

Hypocalcemia commonly presents with

A

convulsions, arrhythmias, tetany, and numbness.
Remember: without calcium, CATs go numb.

174
Q

Hyperkalemia is generally defined as serum potassium levels greater than

A

5.5 mEq/L

175
Q

Hypokalemia is generally defined as serum potassium levels less than

A

3.5 mEq/L

176
Q

↓↑Potassium (Hyperkalaemia and Hypokalaemia)

A

Overview Potassium (K+) is an important ion in the body. K+ is found mainly intracellularly (inside the cells) whereas sodium (Na+) is found extracellularly (outside the cells).

  • Serum Potassium: 3.5mmol/L - 5.0mmol/L
  • Serum Sodium:

Therefore:

  • Hyperkalaemia: >5mmol/L
  • Hypokalaemia: <3.5mmol/L

As the pH rises , K+ is shifted intracellularly and the serum levels falls; conversely when serum pH decreases, intracellular K+ shits extracellularly into the vascular space and so the serum level increases. This is because H+ and K+ are both positive and it is important to have normal +ions levels in the serum to maintain a gradient across the cell membrane to maintain the excitability of nerve and muscle cells, including the myocardium.

177
Q

Transcellular shifts as

A
178
Q

Causes of Hyperkalaemia

A
179
Q

Signs and symptoms hyperkalaemia

A
180
Q

Management hyperkalaemia

A
181
Q

MANAGEMENT OF HYPERKALAEMIA DEPENDING ON SEVERITY

A
182
Q

Complications of Hyperkalaemia

A

Cardiac arrest
Weakness
Paraesthesiae
Decreased reflexes
Ascending paralysis

183
Q

Signs and symptoms hypokalaemia

A

Generalised muscle weakness
Respiratory depression
Ascending paralysis
Ileus, constipation
Palpitations, Arrhythmia, Cardiac arrest
Nephrogenic diabetes insipidus (characterised by polyuria and polydipsia)

184
Q

Management hypokalaemia

A

Management - nonpharmacological

  • ECG
  • ABCD
  • Check serum potassium

Management - pharmacological

  • Chlorvescent - Given STAT
  • Slow K
  • Potassium Chloride (KCl) IV given in 10mmol in 100ml of normal saline
  • Check serum potassium
185
Q

ECG findings hypokalaemia

A

Peaked P waves
T wave flattening and inversion
U waves

186
Q

↑↓Na (Hypernaturaemia and Hyponaturemia

A

Overview Hyponatremia is commonly defined as a serum sodium concentration below 130 mmol/L.

  • Defined as a serum Na+ <130mmo/L
  • It affects 1% of hospital in patients (on call book), 15% (BMJ)
  • Most cases require no treatment.
187
Q

↑↓Na (Hypernaturaemia and Hyponaturemia) Classification

A
188
Q

Pseudohyponatraemia (arefactual)

A

Laboratory analysis technique
Hyponatraemia with normal serum osmolality
* Hyperlipidaemia, hyperproteinaemia
Hyponatraemia with increased serum osmolality
Hyperglycaemia, mannitol, excess urea
Toxic alcohols (ethanol, methanol, isopropyl alcohol, ethylene glycol)

189
Q

Hyponatreamia with high urinary Na+

A
190
Q

Hyponaturaemia with low urinary Na+

A
191
Q

Osmotic demyelination syndrome (central pontine myelonosis)

A
  • Rapidly correcting hyponatraemia may produce permanent central nervous system injury, due to osmotic demyelination.
  • Patients with chronic hyponatraemia (ie known duration more than 48 hours) are particularly at risk.
  • Clinical manifestations typically delayed for 2-6 days.

Symptoms include dysarthria, dysphagia, paraparesis or quadriparesis, behavioural disturbances, movement disorders, seizures, lethargy, confusion, disorientation, obtundation, and coma. Severely affected patients may become “locked in”; they are awake but are unable to move or verbally communicate

Clinical Presentation
* Mild-moderate
Lethargy, weakness and ataxia
Nausea and vomiting
Headache
* Severe (<120mmols)
Confusion
Seizures and coma

192
Q

What is the common diagnostic of pheochromocytoma

A

An increase in 24-hour urine levels of metanephrines and catecholamines

193
Q

What is Pheochromocytoma

A

a tumor of the adrenal medulla that is associated with von Hippel-Lindau disease.

194
Q

he 5 presenting features of pheochromocytoma.

A

5 Ps of pheochromocytoma:

Pressure (episodic, elevated diastolic blood pressure)
Pain (pulsatile headache)
Perspiration
Palpitations (paroxysmal tachycardia)
Pallor

195
Q

Carcinoid syndrome results from

A

tumors associated with high levels of serotonin secretion.

196
Q

Carcinoid syndrome is associated with

A

flushing, wheezing, and diarrhea due to increased serotonin secretion

197
Q

The definitive treatment of carcinoid syndrome tumors is

A

surgical resection.

198
Q

Electrolyte disturbance Hypercalcaemia vs hyperkalaemia

A

Sandra Phase 2a (17 decks)

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