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pathology sem 6 > Lecture 3 > Flashcards

Lecture 3 Flashcards

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1
Q

what are microadeonomas

A

less than 1cm, does NOT modify the sella tursica, does not produce pituitary tumour syndrome

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2
Q

what is macroadenoma

A

more than 1cm, produces syndrome of pituitary tumours

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3
Q

what is hyperpituitarism and what are the causes

A

the production of too many hormones form the adenohypophysis (anterior pituitary)
due to :
1) autonomous over production
2) excess production of hypophyseal stimulating factors
3) underproduction of inhibiting factors
4) loss of inhibition following destruction of other endocrine functions

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4
Q

what are some clinical manifestations of hyperpituritarism

A

Artheritis
Chest (barrel)
Rough facial features
Odd sensations
Muscle weakness & fatigue
Enlargement of organs
Growth of coarse hair
Amenorrhea: breast milk production
Loss of vision
Impotence
Snoring

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5
Q

what is acromegaly

A

excess GH in adults, caused by pituitary adenoma. acromegaly in adults and gigantism in juniors.

  • large tongue with deep furrows, deep voice, excessive sweating ( diaphoresis) insulin resistance, HTN.
  • diagnosis: Increases serum IGF , failure to suppress GH, pituitary mass seen on brain MRI.

-Treatment: pituitary adenoma resection, treat with octerotide or dopamine agonists.

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6
Q

where are the posterior pituitary hormones stored and produces and give some examples

A

stored: posterior pituitary
produced: hypothalamus.

e.g ADH ( fluid control balance, controls renal absorption and has vasoconstriction properties) , oxytocin

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7
Q

what happens if we have increased and decreased oxytocin ( PPD)

A

increased: excess milk production, precipitates childbirth
decreased: prolonged childbirth, diminished milk

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8
Q

what happens if we have increased and decreased ADH ( PPD)

A

increased: Increased BP, decreased urinary output, edema, SIADH
decreased: diabetes insipidus, dialute urine and increased urine output

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9
Q

what is posterior pituitary syndrome

A

excess ADH (abnormal reabsorption of water, inability to excrete diluted urine)
caused by ectopic ADH secretion
- non endocrine neoplasm
- non neoplastic pulmonary disease
- primary CNS lesions

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10
Q

what are the thyroid function blood tests

A

TSH 0.4 –5.0 mU/L
Free T4 (thyroxine) 9.1 – 23.8 pM
Free T3 (triiodothyronine) 2.23-5.3 pM

The main tests to be done is TSH and free T4

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11
Q

what is hashimotos disease

A

HYPOthyroidism
autoimmune lymphocytic thyroiditis
more common in females than males
runs in families
- autoimmune disease when the immune system reacts against thyroid antigens
- progressive depletion of thymocytes which are gradually replaced by mononuclear cell infiltration
- sensitisation of auto reactive CD4+ t helper cells to thyroid antigens is the initiating event

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12
Q

signs and symptoms of hashimotos thyroiditis

A
  • non specific
  • mostly to do with ageing
  • subtle symptoms
  • metabolic slowing of the body
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13
Q

what is subacute thyroiditis

A
  • a viral infection
  • infiltration of granulomas on the gland
  • painful goitre
  • hyperthyroidism phase
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14
Q

hyperthyroidism and cause

A

increase thyroid levels
high T4 and high T3
low TSH

CAUSED:
- Graves disease is a cause of hyperthyroidism
over treatment with thyroxine,
- transient neonatal thyrotoxicosis: when the mother. has graves disease and her antibodies might cross the placenta and stimulate thyroid function but at the age of 4-6 months. is disappears without treatment

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15
Q

what is graves disease

A
  • Most common cause of hyperthyroidism
  • TSH-R antibody (stimulating)
  • Main presentation: Goitre, proptosis

overproduction of IgG antibodie, directed against TSH, so it stimulated thyroid hormone production as it acts on the thyroid receptors. consequently is causes a gaiter formation, there are genetic and environmental causes
- caucasian association with: HLAB8, DR3,DR2

clinical features: thyroid enlargement, occurs between 30-50 year olds, ophthalmopathy (eyes)

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16
Q

hypothyroidism vs hyperthyroidism

A

hypo - cold intolerance, decreased sweating, weight gain, dry skin, brittle hair, brittle nails. preorbital edema. constipation, uterine blessing, fatigue, Bradycardia
hyper - heat intolerance, increased sweating, wight loss, increased basal metabolic rate, warm moist skin, fine hair, ophthalmonopathy, diarrhoea, uterine bleeding, hyperactivity, tachycardia

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17
Q

what is subacute lymphocytic thyroiditis

A

usually in a postpartum patient during the first 3 months of delivery and lasts 1/2 months, and if they have has it before during pregnancy there is a risk of reoccurrence for subsequent pregnancies.

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18
Q

what is diffuse and multi nodular goiters

A

impair synthesis of thyroid hormones, impairment causes increase in TSH levels and so enlargement of gland

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19
Q

folicular adenoma of thyroid gland ( benign)

A
  • benign
  • follicular cell differentiation
  • cold nodule
  • most common thyroid neoplasm
  • normal thyroid tissue
  • encountered in 4th and 5th decades
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20
Q

papillary carcinoma

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A
  • arises from follicular cells of thyroid gland
  • most common form of thyroid carcinoma
  • occurs in 30- 50 years of life
  • exposure to ionising radiation
21
Q

folicular carcinoma

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A

Also arises from follicular cells of thyroid gland.
more common in women
painless solitary nodule ( like papillary) present In older age.
diagnosis mean age 50+
lacks psammoma bodies

22
Q

anapaestic carcinoma

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A

least common
most aggressive and the worse
rapid growth, hoarseness and dyspnea
large invasive tumor

23
Q

medullar thyroid cancer clinical symptoms

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A

lump at base of neck, difficulty swallowing
- locally advanced disease
- diarrhoea
- paraneoplasric syndromes including Cushings

medullary thyroid cancer produced calcintonin and elevated levels of it.

24
Q

what Is hyperparathyroidism

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A

we have primary and secondary
primary: unknown cause through adenomas and hyperplasia
secondary: occurs in chronic kidney disease or vitamin D deficiency, PTH levels are raised by calcium levels are low. or normal
tertiary: longstanding renal failure

25
primary hyperparathyroidism
hypertension - renal involvement - increased cardiovascular mortality gastrointestinal - peptic ulcer - anorexia, nausea, vomiting, constipation - pancreatitis due to pancreatic duct stone
26
secondary hyperparathyroidism
excessive secretion of parathyroid hormones (PTH) in response to hypocalcemia, hyperphsophatemia - associated with hypertrophy of glands - seen in chronic kidney disease - a result of malabsorption ( small bowel syndrome, chronic pancreatitis) - elevated PTH, if phosphorus is elevated it is due to renal - if phosphorus is Low, it is due to vitamin D deficiency - prevent via: vitamins D replacement - surgery
27
what is HYPOparathyroidism
occurs due to hypo secretion of PTH by parathyroid gland, decrease in calcium level and hyperphosphetemia, etiological cause -> decreased gland function -> resistance to PTH -> inadequate OTH secretion and increased reabsorption of Ca+ in GI tract -> blood calcium drops -> muscular irritability -> uncontrolled spasm
28
etiology of hypopaprathyroisism
- tumor of thyroid gland - following a thyroidectomy - accidental removal of parathyroid gland - idiopathic causes - inadequate secretion of PTH - increased reabsorption of calcium in GI tract - phosphate excretion by the kidneys decreases
29
hypothyroidism signs and symptoms
low serum calcium low PTH levels
30
what is adreocortical hyperfunction (hyperadrenealism) the syndromes
- cushings - hyperaldosteronism - adrenogenital caused by excess of androgens
31
cushings syndrome causes (hyperfunction of aderenocortical)
most cases are caused by the administration of exogenous glucocorticoids, or via primary hypothalamic pituitary diseases associated with hyper secretion of ACTH. ACTH dependent: pituitary CRH _ secreting neoplasms ACTH independent causes: adrenal carcinoma. adrenal adenoma pseudo-bushings syndrome - glucocorticoid administration
32
pathophysiology of cushings
etiological factor -> normal feedback mechanisms that control adrenocortical functions are ineffective -> excesss secretion of adrenal cortical hormones -> inadequate amount of adrenal cortical hormones in secretion -> hypercortisolim
33
what do we see in someone that has bushings syndrome
fat deposits in cheeks (moon face) - purple striae ( loss of collage, thin skin) - poor wound healing - hyperglycaemia - osteoporosis - muscular weakness - hisitism
34
primary hyperaldosteronism (conns disease)
caused by problem within the adrenal glands, caused by benign tumour of adrenal glad. symptoms: tiredness, muscle weakness, polyuria, mood disturbance, muscle cramps, resistant hypertension, metabolic alkalosis, hypokkalemia. causes: bilateral adrenal hyperplasia, glucocorticoid remediable aldosteroism,
35
adrenogenital syndrome
aka congenital adrenal hyperplasia _> caused by inherited enzyme deficiency, in adrenal cortex leading to altered levels of. adrenal cortical hormones like mineralocorticoids etc the syndrome occurs when an enzyme deficiency leads to decreased adrenal synthesis of glucocorticoid which impairs feedback inhibition n the pituitary. excessive production of sex hormones
36
adrenogenital syndrome symptoms in males and females
males before birth: enlarged external genitals in childhood: premature sexual development, enlarged penis, short, pubic hair adulthood: increase sex drive and muscular power females: before birth: enlarged clitoris and labia in childhood: no development of sexual characteristics, no enlargement of breasts - deep voice - muscular growth adulthood: hisutism ( hair growth), atrophy of uterus and breast, homosexuality
37
adrenal insufficiency
impairment in synthesis and release of adrenocortical hormones primary -> results from. disease intrinsic to adrenal cortex secondary -> results from impaired release or ACTH from pituitary gland tertiary -> results from the impaired release of corticotropin releasing hormone from hypothalamus.
38
acute adrenal insufficiency
observed in patients with primary AI pastoral hypotension may progress to hypovolmic shock may resemble neurologic disease adrenal crisis can be triggered by an intercurrent illness, surgical stress, infection
39
chronic adrenal insufficiency
non specific signs and symptoms like fatigue we have hyperpigmentation, cause dry excess ACTH stimulation of melanocytes, worsens through sunlight skin has an alabaster like paleness due to lack of ACTH secretion
40
what is Addisons disease (cause and diagnosis too)
adrenal insufficiency, when the body does not produce enough of certain hormones, adrenal glands produce too little cortisol and aldosterone primary causes: autoimmune disease, body mistakes an organ for an invader - prolonged administration of glucocotricosteroids - body infections - cancers -blood thinners diagnosis: blood tests (measure cortisol etc) X rays
41
complications of Addisons disease
hypertension can lead to shock, circulatory collapse, pain in lower back or legs, GI manifestations e.g vommiting, diarrhoea
42
clinical presentations of adrenocortical carcinoma
- weight gain in face, neck and trunk of body - growth of fine hairs on face, upper back or arms - moon face - lump of fact on back of neck - deep voice and sweeping of sex organs - muscle weakness - high blood sugar - high blood pressure
43
what is incidentaloma
unapparent mass detected incidentally by imaging studies conducted for other reasons
44
pheochromocytoma
etiology: most common tumor of adrenal medulla, associated with germline mutations the tumor secretes norepinephrine, dopamine which can cause episodic hypertension
45
what is the pineal gland
attached to roof of 3rd ventricle, breath the posterior end of corpus callosum after 7 years of age it shrinks physiological function of maintaining circadian rhythm synthesises melatonin from seratonin during night
46
pineal gland disease
- tumors - injuries to pineal gland - pineal gland calsification: calcium accumulates - obstruction of third ventricle SADS (seasonal affective disorder) hyper secretion of melatonin, symptoms: cells prepare for winter, sleepy, sad, tired, weight gain, depression
47
hypoglycemia
low blood sugar normal range: 70-110mg/dL it is not a disease itself but an indicator of health problems
48
hypoglycemia pathophysiology
PATHOPHYSIO: in diabetes it does not occur, to defend, we can have an increased release of glucagon, epinephrine, cortisol glucagon stimulates both gluconeogenisis and glyconeolysis epinephrine stimulates it too via acting on beta andrenogenic receptors cortisol and growth hormone contribute only after prolonged hypoglycemia 1) failture to receive or absorb nutrient 2) less production or release of hepatic glycogen 3) limited substrate for gluconeogensis 4) less alternative fuel production 5) increased utilisation of glucose
49

pathology sem 6 (13 decks)

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