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patho II > Endocrine system I (a) > Flashcards

Endocrine system I (a) Flashcards

1
Q

Hyperglycemia resutls from?

A

(high blood sugar) defects in insulin
secretion, insulin action, or both

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2
Q

diganosis of Diabetes Mellitus

A

1) fasting blood sugar of ≥ 126mg/dL or,
2) Random blood glucose conc. of ≥ 200mg/dL, [with classical signs and symptoms] or,
3) Abnormal oral glucose tolerance test, with a
glucose concentration of ≥ 200mg/dL, two hours
after a standard carbohydrate load

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3
Q

*

The 5 major complications of Diabetes Mellitus (give examples)

A

1) Retionopathy (Cataracts, Galucoma)
2) Nephropathy (Glomeroulonecrosis, pyelonephritis)
3) Neuropathy (peipheral-nerves / autonomic-bladder)
4) microangiopathy (Hemorrhage, cerebral vascular infarcts-stroke)
5) Macrovascular disease (Atherosclerosis, MI)

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4
Q

*

clinical features of Diabetes Mellitus

A
  1. “Honeymoon period”: First 1-2 years after
    manifestation of overt type 1 diabetes
  2. Hyperglycaemia
  3. Glycosuria –> Osmotic Diuresis –> Polyuria
  4. Polydipsia (increased thirst)
  5. Polyphagia (excessive hunger)
  6. Ketoacidosis (severe cases) [type 1 DM]
  7. Hyperosmolar non-ketotic coma (sever dehydration) [type 2 DM]
  8. Weight loss [type 1 DM]
  9. Obesity [type 2 DM]

honeymoon : pancreas is still able to produce small amounts of insulin

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5
Q

Epi + Primary defect of Type 1 Diabetes

A
  • Autoimmune T-cell mediated destruction of pancreatic β-cells
  • absolute insuline deficiency

Epi : < 20 yrs

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6
Q

Epi + Primary defect of Type 2 Diabetes

A
  • increase in Insulin resistance
  • progressive pancreatic β-cell failure
  • realitive insuline deficiency

Epi : > 40yrs , overweight patients

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7
Q

Histology of Type 1 vs Type 2 diabtes Mellitus

A

Type 1: “insulitis” ; Islets lymphocytic infiltrates (made up of macrophages and lymphocytes)
Type 2: Islet Amyloid polypeptide (IAPP) deposists

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8
Q

Type 1 vs Type 2 diabetes

A
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9
Q

Explain the mechanisms responsible for β-cell dysfunction and insulin resistance in Type 2 DM

A

1) Free fatty Acids (FFAs) –> cause β-cell dysfunction –>
2) Induces insulin resistance in target tissues –>
3) Induce secretion of Pro-inflammatory Cytokines

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10
Q

Explain the Pathology of how islets are replaced by Amyloid in Type 2 DM

A

1) inadequate compensation for peripheral resiatnce –> Hyperglycaemia + loss of β-cell mass
2) Excess FFAs and glucose –> lymphocytic infiltration (Recruitment of macrophages and T cells) –> Cytokine production –> Beta cell dysfunction and death
3) Replacement of islets by amyloid

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11
Q

what is the normal body mechanism to increased insulin secretion

A

increased insulin secretion –> Compensation for Peripheral resistance –> Maintenance of normal plasma glucose

       NOTE: diabetic pateints have Inadequate (insufficient)
				 compensation for peripheral resistance
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12
Q

list 4 Diabetic Macrovascular diseases

A

1) MI
2) Atherosclerosis of the aorta and large/medium-sized arteries
3) Gangrene of the lowere extremities
4) Hylaine Arteriosclerosis [associated with hypertension]

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13
Q

list 3 complications of Diabetic Microangiopathy

A

1) Diabetic Nephropathy (Glomerulosclerosis, Pyelonephritis, Hylaine Arteriolosclerosis)
2) Retinopathy (cataracts, Galucoma)
3) Neuropathy (nerve injury in the legs and feet)

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14
Q

Diabetic Nephropathy

poorly controlled diabetes can cause damage to blood vessel clusters , leading to Glomerular lesions –> kidney damage. Explain how this happens

A

Changes in the apperance of the glomerulus due to lesions:
GBM thickening –> Mesangial expansion (Diffuse mesangial sclerosis) –> Nodular glomerulo-sclerosis (Kimmelstiel-Wilson lesions) –> Diffuse glomeurlosclerosis (chronic)–> kidney damage due to Ischaemia

* GBM : Glomerular Basement Membrane

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15
Q

Kimmelstiel-Wilson Lesion is aka?

A

Nodular Glomerulosclerosis

  • Ball-like deposits, at the glomerular periphery
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16
Q

ocular complications of Diabetes

A

i. Retinopathy (Proliferative/ Non-proliferative)
ii. Cataract formation
iii. Glaucoma

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17
Q

Non-proliferative vs Proliferative Diabetic Retionopathy

A

Non-proliferative
–> Microangiopathy,retinal haemorrhages and exudates (“soft” = microinfarcts, “hard” = deposits of plasma proteins and lipids), micro-aneurysms and oedema

Proliferative:
–> Process of neovascularisation and fibrosis; Vitreous haemorrhages, due to rupture of newly formed vessels –> Organisation of the haemorrhage –> Retinal detachment

*Vitreous Haemorrhage : presence of blood in the vitreous humor

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18
Q

The 3 forms of Diabetic Neuropathy

A

1. Peripheral, Symmetric Neuropathy of the
lower extremities –> Disturbance of both motor and sensory function
2. Autonomic Neuropathy –> Disturbance of
bowel and bladder function
3. Diabetic Mononeuropathy –> Sudden footdrop, wrist-drop or isolated cranial nerve palsies

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19
Q

The 2 PanNETs associated with MEN-1 syndrom (mutation)

*PanNETs: Pancreatic Neuro-Endocrine Tumours

A

1) Insulinomas (in the pancerase)
2) Zollinger-Ellison Syndrome (Gastrinomas)

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20
Q

location of Insulinomas

A

pancrease

21
Q

location of Gastrinomas (Zollinger-Ellison syn.)

A

Gastrinoma triangle:
* Duodenum
* Peri-Pancreatic soft tissues
* Pancreas

22
Q

Clincal features of Zollinger-Ellison Syn.

A

1) Hypergastrinaemia –> ↑ gastric acid secretion –> peptic ulceration
2) Peptic ulcer
3) Diarrhoea (in > 50% of patients)

23
Q

clinical manifesations of Insulinomas

A

1) Attacks of Hypoglycaemia (low blood sugar)
2) CNS manifestations
Confusion
Stupor (state of near-unconsciousness)
Loss of consciousness

24
Q

Macroscopic Features:
* Small, <2cm
* Most common, solitary lesions
* Localised to the pancreas

Microscopic Findings:
* Regular cords of monotonous cells (large cells)
* Orientation to the vasculature
* Amyloid deposits in the extracellular tissue

Are the features of what type of PanNET?

A

Insulinoma

25
Q

primary causes of Thyrotoxicoses associated w/ Hyperthyrodism

A

1) Diffuse toxic hyperplasia (Grave’s disease)
2) Hyper-functioning (“toxic”) multi-nodular goiter
3) Hyper-functioning (“toxic”) adenoma
4) Iodine-induced hyperthyroidism

26
Q

secondary causes of Thyrotoxicoses associated w/ Hyperthyrodism

A

TSH-secreting pituitary adenoma (rare)

27
Q

diagnostic tests for Hyperthyroidism

A
  1. increased T3/T4
  2. Decreased TSH (if Primary)
28
Q

Measurement of radioactive iodine uptake by the
thyroid gland
* Diffusely [increased/decreased] uptake in Grave’s disease
* [Increased/decreased]uptake in a solitary nodule in toxic adenoma
* [Increased /decreased] uptake in thyroiditis

A
  • Diffusely increased uptake in Grave’s disease
  • Increaseduptake in a solitary nodule in toxic adenoma
  • [decreased] uptake in thyroiditis
28
Q

clinical features of Cretinism

A
  • Impaired development of skeletal and
    central nervous system
  • Short stature
  • Coarse facial features
  • Protruding tongue
29
Q

clinical features of Gull disease (Myxoedema)

A
  • Generalised apathy
  • Mental sluggishness
  • Cold intolerance
  • Obesity
  • Enlargement of the tongue
  • Deepening of the voice
  • Constipation
  • Heart enlargement and pericardial effusions

* type of hypothyroidism

30
Q

LABs of Primary vs secondary Hypothyroidism

A

Primary Hypothyroidism:
* Increased TSH
* Decreased serum T4

Secondary Hypothyroidism:
* Not increased TSH
* Decreased serum T4

31
Q

casues of Hypothyroidism

A
  • Primary: Intrinsic abnormality in the thyroid
  • Secondary: Primary Hypothalamic or Pituitary disease
32
Q

Types of Thyroiditis

A

 Chronic Lymphocytic (or Hashimoto) Thyroiditis
 Granulomatous (de Quervain) Thyroiditis
 Subacute Lymphocytic Thyroiditis
 Riedel (Fibrous or Invasive) Thyroiditis

33
Q

Chronic Lymphocytic (Hashimoto) Thyroiditis.
Linkage to ————— gene cytotoxic

A

Cytotoxic T-lymphocyte-associated Ag-4
gene (CTLA4)

34
Q

Microscopic Findings:
* Inflammatory infiltrates (lymphocytes, plasma cells) + Germinal centers
* Atrophic thyroid follicles, lined by Hürthle or Oxyphil cells (marked eosinophil., granular cytopl.)

features of?

A

Chronic Lymphocytic
(Hashimoto) Thyroiditis

35
Q

CF of Hashimoto Thyroiditis

A

Painless, symmetric and diffuse enlargement of the thyroid

36
Q

(Hashimoto) Thyroiditis is associated with?

A

hypothyroidism (gradual development)

37
Q

complications of Chronic Lymphocytic
(Hashimoto) Thyroiditis

A

Increased risk for development of B-cell non -Hodgkin lymphomas, within the thyroid gland

38
Q

causes of Subacute Granulomatous
(de Quervain) Thyroiditis

A
  • Viral infection
  • Inflammatory process triggered by viral infections;
    commonly, history of upper respiratory tract
    infection
39
Q

Microscopic Findings:
* Disruption of thyroid follicles –> Extravasation of
colloid –> Polymorphonuclear infiltrate –>
Lymphocytes, plasma cells and macrophages
* Development of a granulomatous reaction with
giant cells –> Granulomatous inflammation
* Healing: Resolution of inflammation and fibrosis

Macroscopic features :
- firm gland
- Intact capsule
Features of?

A

SubacuteGranulomatous
(de Quervain) Thyroiditis

40
Q

CF of Subacute Granulomatous
(de Quervain) Thyroiditis

A
  • Neck pain (particularly with swallowing)
  • Fever
  • Malaise
  • Transient Hyperthyroidism –> Transient
    Hypothyroidism –> Euthyroid state
    (within 6-8 weeks)
41
Q

casuse of Silent or painless Thyroiditis

A

Autoimmune

42
Q

CF of silent or painless Thyroiditis (Subacute Lymphocytic Thyroiditis)

A
  • Painless neck mass
  • Thyrotoxicosis (initially) –> Euthyroid state
    (within a few months)
43
Q

Macroscopic Features:
* Mild symmetric enlargement of the thyroid gland

Microscopic Findings:
* Lymphocytic infiltrates and hyperplastic germinal centers

Features of?

A

Subacute Lymphocytic Thyroiditis (aka silent or painless Thyroiditi)

44
Q

Riedel Thyroiditis is aka?

A

Fibrous Thyroiditis, Invasive Thyroiditis

45
Q

Riedel Thyroiditis has a Relation to a group of idiopathic systemic disorders known as —————–?

A

Inflammatory Fibrosclerosis

46
Q

CF of Riedel Thyroiditis (Fibrous/Invasive Thyroiditis)

A
  • Hard and fixed thyroid mass
47
Q

Microscopic findings:
* Thyroid replaced by fibrous tissue and inflammatory infiltrate (plasma cells , lymphocytes, macrophages)

Features of?

A

Riedel Thyroiditis

patho II (29 decks)

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