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imed3004 COPY > Path (AP): Endocrine pancreas & diabetes (MD) > Flashcards

Path (AP): Endocrine pancreas & diabetes (MD) Flashcards

1
Q

What are the most common adrenocortical neoplasms?

A

Adrenocortical adenomas

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2
Q

What are the accompanying results of adrenocortical adenomas?

A

Well circumscribed, nodular

Non-functional. (If functional associated with atrophy of non-neoplastic gland)

Lots of fat tissue

Proliferation of cells similar to those of adrenal cortex

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3
Q

What are adrenocortical carcinomas?

A

Rare, more often functional, tumours of the adrenal cortex.

Need to be differentiated from metastatic malignancies.

Large invasive neoplasms with necrosis and haemorrhage

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4
Q

What causes hyperaldosteronism?

A

Primary: Autonomous overproduction due to noplasms, or idiopathic causes.

Secondary: Response to RAS system. Decreased renal perfusion, arterial hypovolaemia and oedema, pregnancy.

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5
Q

What causes excess androgen production?

A

2 settings:

Adrenocortical neoplasms

Congenital adrenal hyperplasia

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6
Q

What causes congenital adrenal hyperplasia?

A

Autosomal recessive defects in steroid biosynthesis

Channeling of steroid precursors into other pathways

Reduction in cortisol production

Masculinisation

Some may result in aldosterone deficiency

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7
Q

What causes secondary adrenocortical insufficiency?

A

Any disorder of the hypothalamus of pituitary that reduces output of ACTH.

Can be caused by prolonged corticosteroid administration

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8
Q

What are the most common tumours of the adrenal medulla?

A

Neural or neuroendoncrine tumours:

Adrenal phaeochromocytoma

Neuroblastoma

Ganglioneuroblastoma

Ganglioneuroma

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9
Q

What is the origin of the adrenal medulla? What does it do?

A

Neural crest origin (ectoderm) it produces adrenaline and noradrenaline

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10
Q

What are phaeochromocytes?

A

Neuroendocrine cells

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11
Q

How are cells of the adrenal medulla arranged?

A

In clusters supported by a delicate fibrovascular stroma

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12
Q

What is the tumour that arises from adrenal medullary neuroendocrine cells called?

A

Adrenal phaeochromocytoma

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13
Q

What is neoplasm that resembles adrenal phaeochromocytoma which is involved in autonomic NS in head and neck called? What anatomical structures does it involve?

A

Paraganglioma, it includes carotid body (baroreceptors), vagus nerve, aorta, and its branches

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14
Q

How does adrenal phaeochromocytoma arise?

A

Can be sporadic or familial. (associated with some familial syndromes such as von hippel-lindau))

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15
Q

What happens in adrenal phaeochromocytoma?

A

Most are benign and can be secretory or non-secretory.

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16
Q

How can adrenal phaeochromocytoma be diagnosed?

A

May be secretory producing more adrenaline/noradrenaline

Can cause paroxysmal or persistent hypertension, headaches, sweating, palpitations, fatigue, GI and cardiac symptoms, tremors.

Imaging: Adrenal mass, variable size, up to several kgs.

Biochemistry: Secretion of free catecholamines and their metabolites in urine

Histopathology: Zellballen, neuroendocrine markers

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17
Q

What is zellballen?

A

Nest-like clusters of uniform, round-to-polygonal chief cells surrounded by delicate richly vascular tissue and sustentacular cells, a pattern characteristic of paraganglioma

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18
Q

What people should be monitored carefully for endocrine tumours?

A

Patients who present with vague, protean symptoms.

When choosing to treat or withdraw steroids exercise caution in these people.

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19
Q

What are the endocrine cells of the pancreas and what do they produce?

A

Alpha - glucagon

Beta - Insulin

Delta - Somatostatin (suppress both insulin and glucagon)

PP - Pancreatic polypeptide

2 minor types:

D1 - Vasoactive intestinal polypeptide (VIP), induces glycogenolysis and hyperglycaemia

Enterochromaffin cells - Serotonin

20
Q

What are the Australian Diabetes Society criteria for diagnosis of diabetes??

A

Fasting (>8 hours) plasma glucose > 126 mg/dl (7mmol/L)

Random plasma glucose >= 200 mg/dl

2-hour plasma glucose >= 200mg/dl with loading dose of 75g

Glycated haemoglobin (HbA1C) >=6.5%

21
Q

What causes type 1 diabetes?

A

Destruction of beta cells causing total or near total insulin deficiency.

22
Q

What age do people generally get type 1 diabetes?

A

<20 years

23
Q

What causes type 2 diabetes?

A

Peripheral resistance to insulin and subsequent inadequate insulin secretion.

Usually adult onset but not universal

24
Q

What stage develops prior to full blown diabetes?

A

Impaired glucose tolerance which results in elevated plasma glucose but not in the diagnostic range.

25% develop T2DM within 5 years

25
Q

What is Type 1.5 or 1a diabetes?

A

Up to 10% of adults with T2DM have islet autoantibodies, particularly if non-obese

26
Q

What are the possible risk factors to type 2 diabetes?

A

Drugs (Glucocorticoids, thyroid hormone, interferon, etc)

Exocrine pancreatic damage (chronic pancreatitis, pancreatectomy, trauma, neoplasia, etc)

Gestational DM

Endocrinopathies (Cushing’s hyperthyroidism, acromegaly, phaechromocytoma, etc)

Genetic defects in beta cell function

Infections (rubella, CMV, Coxsachie B)

Genetic syndromes

27
Q

How does DM clinically present?

A

T1: Indolent onset with sudden presentation. (Without exogenous insulin patients end up ketotic which leads to coma and then death)

T2: Unexplained fatigue, dizziness, blurred vision. Can often be asymptomatic and may result in hyperosmolar non-ketotic state

28
Q

How does T1 diabetes happen? (pathogenesis)

A

Develops in childhood, manifests at puberty, progresses with age.

Interplay of genetics (especially at HLA-DR3 or HLA-DR4) and environment (still unclear).

Beta cell destruction is a result of loss of self tolerance for T cell specific islet antigens (Autoreactive T cells are not removed and instead attack islets)

29
Q

How does T2 diabetes happen? (pathogenesis)

A

Interplay of genetics (multiple loci, all with small to moderate increases in risk) and environment.(central/visceral obesity, and a sedentary lifestyle)

Develops in adulthood and progresses really slowly. Initially high insulin but peripheral insulin resistance. Later low insulin due to beta cell dysfunction.

Insulin sensitivity decreases due to: FFAs, Adipokines (from adipocytes), inflammation (pro-inflammatory cytokines secreted in response to nutrient excess).

This results in beta cell dysfunction develops later as cells exhaust their capacity to increase secretion.

30
Q

What is gestational diabetes caused by?

A

2 ways:

Patients with pre-existing DM may become pregnant.

Pregnancy may result in impaired glucose tolerance.

31
Q

What is gestational diabetes?

A

High blood sugar that occurs during pregnancy. (Typically resolves following delivery)

32
Q

What are the risks that arise from gestational diabetes?

A

Associated with increased risk of stillbirth and congenital malformations in the foetus, especially macrosomia.

Also associated with increased risk of obesity and diabetes later in life (both mother and the baby)

33
Q

Who is most likely to suffer from gestational diabetes?

A

Obese women more likely than other women.

34
Q

What does insulin do in adipose tissue, the liver, and in muscle?

A

Adipose tissue: Increase glucose update and lipgenesis

Striated muscle: Increases glucose uptake, and glycogen + protein synthesis

Liver: Increases lipogenesis, glycogen synthesis and decreases gluconeogenesis.

35
Q

How is the pathology different in T1 and T2?

A

T1: Inflammatory infiltrate, islet depletion, atrophy.

T2: Amyloid deposition in islets, mild depletion.

36
Q

What are the possible acute complications of diabetes?

A

Ketoacidosis (rare in T2DM)

Hypoglycaemia

Hyperosmolar hyperosmotic state (previously hyperosmolar non-ketotic coma: HONKC)

37
Q

What happens in ketoacidosis?

A

Insufficient insulin causes hyperglycaemia which activates ketogenic pathway, if urinary excretion is compromised this results in systemic ketoacidosis, laboured breathing, ketotic breath and loss of consciousness/coma)

38
Q

What happens in hyperosmolar hyperosmotic state?

A

Usually occurs in T2, it causes severe dehydration due to severe osmotic diuresis due to hyperglycaemia but without the ketosis or acidosis

39
Q

What causes hypoglycaemia?

A

Overtreatment of hyperglycaemia

40
Q

What are the symptoms of hypoglycaemia?

A

Dizziness, tachycardia, confusion, palpitations, potentially loss of consciousness

41
Q

What are the chronic complications of diabetes?

A

Systemic (infections and atherosclerosis)

Brain (Cerebrovascular disease)

Eyes (haemorrhage and exudates)

CVS (Ischaemic heart disease)

PNS (Peripheral neuropathy, poly or mono neuropathy, autonomic dysfunction)

Renal (Diabetic nephropathy, nodular and diffuse glomerulosclerosis, pyelonephritis and papillary necrosis, hyaline arteriolosclerosis, nephrosclerosis)

Skin (Necrobiosis lipoidica, trophic ulceration, gangrene)

42
Q

What causes the chronic complications in diabetes?

A

Majority of chronic complications are due to hyperglycaemia induced vascular damage and/or susceptibility to infection.

This is due to:

Formation of advanced glycation end products

Activation of protein kinase C

Oxidative stress and disturbances in polyol pathways

Hexosamine pathways and generation of F6P

43
Q

How are the diabetic angiopathies grouped?

A

Macroangiopathy: Atherosclerosis, Ischaemic heart disease, cerebrovascular disease, peripheral vascular disease

Microangiopathy: Retinopathy, nephropathy, and neuropathy.

44
Q

Why does diabetes cause an increase in the incidence of infections?

A

Due to impaired cytokine production, WBC production, and reduces blood supply to many areas.

45
Q

What are the main types of renal problems caused by diabetes?

A

Glomerular lesions: Nodular glomerulosclerosis (Kimmelstiel Wilson lesion), diffuse mesangial sclerosis, Glomerular capillary basement membrane thickening.

Renal vascular lesions: Diabetic microangiopathy, Renal artery atherosclerosis

Tubular/Parenchymal lesions: Pyelonephritis and necrotising papillitis, glycogen/lipid vacuoles in tubules

imed3004 COPY (50 decks)

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