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Pathophysiology > unit 8 > Flashcards

unit 8 Flashcards

1
Q

Endocrine Overview

A

Endocrine Disorders Can Arise When:

  • Hormone is secreted to excess
  • Hormone deficiency is present
  • Target cells for the hormone are dysfunctional
  • Hereditary or congenital defects affect endocrine secretions
  • Blood supply to and endocrine tissue is affected
  • Endocrine tissue has undergone hyperplasia
  • Endocrine disorders are most commonly

Endocrine disorders are most commonly caused by tumour in the endocrine tissue:

  • Usually begin
  • Can be functional (–> oversecretion disorder)
  • Can damage endocrine tissues (–> hormone deficiency)

Signs and Symtpoms of an Endocrine Disorder Reflect:

  • Physiologic actions of the hormone
  • Effects of tumour (if tumour is etiologic agent)
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2
Q

Describe Goitre

A
  • Old french ‘goitron’ (gullet) or latin ‘guttur’ (throat)
  • Enlargement of the thyroid gland that may be visible as a swelling in the throat area
  • Clinical sign of thyroid gland dysfunction
  • Goitre can occur from hypo or hyper thyroidism
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3
Q

Describe Hyposecretion (endemic) Goitre

A
  • Low endemic iodine levels in soil and food

- Cannot have normal T3 and T4 production

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4
Q

Describe Hypersecretion (toxic) Goitre

A
  • Iodine levels are not limited
  • Thyroid gland is over stimulated therefore, excessive T3 and T4 production produces toxic effects
  • May be due to excessive TSH stimulation ex: by substances as goitrogens
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5
Q

Describe Goitrogens and Goitre

A

Goitrogens are substances that block T3 and T4 secretion:
–> TSH levels rise –> TSH Causes thyroid hyperplasia (goitre)

Food goitrogens prmote goitre when ingested in large amounts (these act directly on the pituitary and stimulate TSH)
-Cabbage and turnips

Some minerals may also act as goitrogens
-lithium and fluoride

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6
Q

Describe Hyperthyroidism: Graves Disease

A

RECALL THYROID HAS EVERYTHING TO DO WITH METABOLISM

Often associated with autoimmune pathophysiology:
-autoantibodies stimulates TSH receptors on thyroid gland

Signs and Symptoms associated with Excess T3 and T4:

  • Hypermetabolism causes heat intolerance and weight loss in despite increased appetite
  • Increased sympathetic activity such as, heart palpitation, tachycardia and hypertension
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7
Q

Grave’s Dx: Exophthalmos

A

Protruding eyes:
-build up of tissues in orbit pushes eyes outward

Staring, unblinking eyes:
-sympathetic stimulation of eyelid muscle

May cause vision loss

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8
Q

Describe Hyperthyroidism: Thyrotoxicosis

A
  • Also called thyroid storm
  • Sudden onset of acute hyperthyroidism
  • Usually precipitated by acute adrenalin episode: may be triggered by surgery or infection (ex: stress_
  • Life threatening because of acute symptoms such as, hyperthermia, tachycardia, hypertension and heart failure
  • Requires immediate tx to prevent death from arrhythmias
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9
Q

Describe Hypothyroidism

A
  • Mild hypothyroidism is common and easily treated
  • Signs and symptoms are generally opposite to hyperthyroidism and reflect hypo metabolism and decreased sympathetic activity
  • Can result in a small or large thyroid
  • Severe hypothyroidism has several manifestations that include hashimoto’s thyroiditis, myxedema and cretinism
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10
Q

Hypothyroidism: Hashimoto’s Thyroiditis

A
  • Autoimmune destruction of thyroid tissue
  • Insidious onset (months or years to detection): slow progression to hypothyroidism
  • Affects between 0.1% and 5% of all adults in western countries and is most commonly seen in middle aged women
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11
Q

Hypothyroidism: Myxedema

A

Severe hypothyroidism in older children or adults

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12
Q

Hypothyroidism: Cretinism

A
  • Severe hypothyroidism during infant or young child development
  • Characterized by deficient brain development: T3 and T4 essential for neuronal development
  • Formerly common in areas with low endemic iodine (himalayan, inland China, Africa, mountains)
  • Other developmental retardation is also evident (T4 and T3 is essential in all cell and tissue metabolism), this can result in decreased feeding (decreased metabolic rate), stunted growth (decreased cellular metabolism), delayed tooth eruption and malocclusion
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13
Q

Adrenal Medulla: Pheochromocytoma

A
  • Located at top of kidneys and is an excessive producion of adrenalin and noradrenalin by adrenal medulla
  • Major cause of secondary hypertension
  • S/S similar to intense sympathetic stimulation such as hypertension, heart palpitations and diaphoresis
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14
Q

Adrenal Cortex: Cushing’s Syndrome

A

Excessive glucocorticoid secretion

May be caused by multiple pathologies:

  • Adrenal adenoma
  • Pituitary adenoma (master/controlling gland of everything, may also release ACTH making excess amounts of cortizol)
  • Paraneoplastic syndrome (tumours somewhere else in the body that is secreting abnormal hormones
  • Iatrogenic
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15
Q

Paraneoplasti:c Cushing’s

A

Tumour is another tissue (ex:lungs) that secretes ACTH

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16
Q

Iatrogenic: Cushing’s

A

Long term chronic glucocorticoid administration:

  • Feedback inhibition of ACTH secretion causes adrenal cortex atrophy
  • Problematic in times of stress (increased cortisol need)
17
Q

Cushing Signs and Symptoms

A

Glucocorticoids have multiple physiological effects

S/S are related to the effects of excessive glucocorticoids (cortisol secretion)

Effects on fat metabolism: redistribution of body fat causes moon face or buffalo hump

Effects on carbohydrates metabolism:

  • Diabetes syndrome due to elevated blood glucose levels
  • Results from glucose sparing effects of cortisol: gluconeogenesis

Effects of accelerated catabolism (breaking down):

  • Fragile skin (due to skin collagen catabolism)
  • Stretch marks (from purple striae)
  • Osteoporosis ( from bone matrix catabolism)
  • Muscle wasting (due to protein catabolism)
  • Overall cortisol has catabolic effects
  • Adrenal Cortical hormone ‘mimicry’:
  • Hypertension (it mimics mineralocorticoid effects causing hypertension)
  • Hirsutism (mimics androgenic effects and causes hirsutism)
  • Acne (mimics androgenic affects and causes acne)

Other Effects include infection (immune suppression) and reduced stress response

18
Q

Describe Addison’s Disease and its Etiology

A

Characterized by hyposecretion of all adrenal cortex hormones:

  • Glucocorticoids (cortisol)
  • Mineralocorticoids (alderstone)
  • Androgens (testosterone)

Etiology:

  • Commonly autoimmune reaction
  • Infection
  • Destructive Tumours
19
Q

Addison’s Dx: Signs and Symptoms

A

Reflect glucocorticoids (cortisol) insufficiency:

  • Hypoglycaemia (decreased glucose mobilization)
  • Poor response to stress (GAS)
  • Fatigue, weight loss, infection (decreased glucose mobilization

Reflect Mineralocorticoid (aldosterone) Insufficiency:

  • Hypertension (loss of Na+ –> loss of H2O –> Low BV)
  • Hypoatremia (reduced blood in Na+)
  • Hyperkalemia (increased blood K+)
  • Cardiac arrhythmias and failure
  • Hyponatremia and hyperkalemia are bad because they lead to cardiac arrhythmias and failure

Reflect Androgen Insufficiency:
-Decreased body hair

Reflect Feedback Increase in ACTH Secretion:
-Hyperpigmentation (elevated ACTH precursor stimulates melanocytes) of the skin an mucosal surface (buccal mucosa)

20
Q

Describe Diabetes Mellitues

A

Diabetes mellitus occurs asa result of insulin deficit

  • Absolute deficit: loss of insulin production (autoimmune condition that is acting on and preventing the production insulin)
  • Relative deficit: impairment of cellular response to insulin

*Increase glucose in the blood

Insulin is an anabolic hormone that

  • Promotes formation of glycogen, protein and lipid
  • Promotes glucose entry into cells except for the brain and excreting muscles
  • Promotes GI absorption of amino acids
  • Promotes glucose utilization by cells (including ATP generation)

Diabetes in on the rise in NA, except further increase in as incidence of obesity rises

Two Forms: type 1 and type 2

21
Q

Type 1 Diabetes

A

Formerly called insulin dependent diabetes mellitus (IDDM) or juvenile diabetes, it is more common in children and adolescents

More severe form

Most likely to cause serious acute complication

Fundamental abnormality in Type 1 diabetes is autoimmune disorder (T-cell mediated), destruction insulin secreting pancreatic Beta Ce;;s (islets of langerhans) and creates an absolute insulin deficit (not enough insulin)

Clinically managed by insulin replacement therapy

22
Q

Type 2 Diabetes

A

Originally called non-insulin dependent diabetes mellitus (NIDDM) or adult onset diabetes. It is usually a disease of over weight adults (although incidence in younger adults is rising)

Fundamental abnormality in Type 2 diabetes in an increased cellular resistance to effects on insulin and creates a relative insulin deficit (insulin present, but cannot act on cells)

Associated abnormalities are decreased insulin production (milk beta cell damage) and increased glucose production by the liver

Clinical management depends upon adjusting insulin need:

  • Diet to reduce glucose intake
  • Exercise promotes more effective glucose utilization
  • Drugs stimulate beta cells to make more insulin

Type 2 is clinically less severe than Type 1, however, both types are associated with long-term complication of diabetes, which are the major causes of morbidity and death from diabetes

23
Q

Diabetes: Diagnostic Tests

A
  • Fasting blood glucose level
  • Glucose tolerance test
  • Glycosylated hemoglobin test (best test), it tests clinical and subclinical diabetes, monitors glucose levels over several months. A1C test (gold standard) is sometimes called the hemoglobin A1c, HbA1c, or glycohemoglobin test
24
Q

Diabetes: Early Pathophysiology

A

Insulin deficit –> decreased glucose utilization

Hyperglycaemia (to much glucose in the blood):
-Non-utilized glucose accumulates

Glucosuria (glucose in urine):
-Filtered load in kidney exceeds capactiy of renal tubules to reabsorb

Polyuria (including nocturia is an increase in urination at night):

  • Urinary glucose causes osmotic diuresis
  • Diuresis causes electrolyte loss

Dehydration:
-Renal water loss and osmotic transfer of water from cells to blood

Polydipsia:
-Water loss increases thirst

Polyphagia:
-Cellular starvation increases appetite

25
Q

Diabetes: Advanced Pathophysiology

A

Ketonemia or Ketoacidosis (ketones in the blood):
-metabolic products of increased fat and protein metabolism accumulate (ketone bodies are often acids)

Ketonuria (ketones in the urine)
-Ketones spill into urine

Decompensated metabolic acidosis:

  • Also known as diabetic ketoacidosis or diabetic coma
  • Dehydration –> lower GFR –> reduced keno excretion
26
Q

Diabetes Signs and Symptoms

A

Related to metabolic effects of hyperglycemia and decreased glucose utilization:

  • Three P’s (polyuria, polydipsia and polyphagia)
  • Fatigue, lethargy (cells are undernourished)
  • Weight loss (fat and muscle catabolism)
  • Fruity breath odour (keno accumulation, esp acetone)
  • Coma (acidosis and neuronal dehydration)
27
Q

Diabetes Complications: Acute and Chronic

A

Acute:

  • Hypoglycemia (Type 1)
  • Diabetic ketoacidosis (DKA) (type 1)
  • Hyperosmolar hyperglycaemic nonketotic coma (type 2)

Chronic:

  • Angiopathy (vascular problems)
  • Neuropathy
  • Infection
  • Cataracts
  • Pregnancy
28
Q

Acute Complications: Hypoglycemia

A

=insulin shock

Complication related to overabundance of insulin:
-Precipitated by factors that mismatch insulin level and glucose ingestion

Effects manifested soon after glucose level falls

Immediate effects are on nervous system because of neural tissue glucose requirements

Neurological Signs: CNS glucose deprivation:

  • Inability to concentrate
  • Slurred speech
  • Lack of coordination
  • Staggering gait
  • Loss of consciousness
  • Seizures
  • Death

Sympathetic NS Signs: Need tp increase glucose:

  • Rapid HR
  • Pallor
  • Anxiety
  • Diaphoresis
  • Tremors
29
Q

Acute Complications: Ketoacidosis

A

Diabetes Ketoacidosis is a complication related to insufficient insulin levels (hyperglycaemia)

  • Error in dosing
  • Unanticipated food or alcohol ingestion
  • Infection/stress increases insulin requirements

Effects manifested over few days

Signs and symptoms related to:

  • Dehydration and reduced vascular volume (increased urine production), these signs include thirst (activation of hypothalamic thirst centre), dry/rough oral mucosa, warm/dry skin, hypotension (reduced BV), pulse rapid/weak (sympathetic response to hypotension), oliguria (reduced production or urine) and CNS depression (decreased blood flow)
  • Metabolic acidosis (metabolism of fats) signs include rapid deep breathing pattern (trying to ventilate CO2), fruity breath odour (presence of acetone), CNS depression (acidosis) and loss of consciousness (decompensated ketoacidosis)
  • Electrolyte imbalance include abdominal cramps, nausea, vomiting and lethargy/weakness
30
Q

Acute Complications: HHNC

A

Hyperosmolar hyperglycemic non-ketoic coma

More common in type 2

Enough insulin to prevent ketoacidosis, but not enough to prevent hyperglycemia

Hyperosmoarity (due to hyperglycemia) causes neuronal dehydration like:

  • Neurological symptoms
  • Muscle weakness
  • Dysarthria (speech problems)
  • Muscular reflex disturbances
31
Q

Chronic Complications: Angiopathy

A

Metabolic abnormalities related to hyperglycaemia lead to arterial degeneration

Both small and large arteries are affected:
Microangiopathy:
-Thickening and hardening of capillary basement membrane and causes obstruction and ruptures capillaries and small arteries
-Effects include ischemia –> necrosis of distal tissues, microaneurisms (damage to BV walls), neovascularization (formation of new blood vessels) and fibrosis (scar tissue formation)
-Consequences: vascular degeneration of glomerulus (diabetic nephropathy) (kidney –> glomerulus filters out blood and toxins: may result in kidney failure), diabetic retinopathy may occur

Macroangiopathy: caused by atherosclerosis and is associated with hyperlipidemia, hypertension and artery damage
-Consequences include MI, cerebrovascular accident (stroke), peripheral ischemia (gangrene and ulcers)

32
Q

Chronic Complications: Neuropathy

A

Central and Peripheral Neuropathy caused by schema and metabolic disruption of myelin

Impaired sensations (particularly in lower extremities)

Parasthesia (numbness, tingling)

Muscle weakness

Muscle wasting

Loss of autonomic controls (incontinence, impotence, diarrhea and dizziness)

33
Q

Chronic Complications: Infection

A

Infection frequent in diabetics because of:

  • Vascular impairments (decreased tissue resistance)
  • Delayed healing (insulin deficit –> cellular dysfunction)
  • Hyperglycemia (nutrient source for microorganisms)

Common Infections:

  • Cutaneous, oral, vaginal candidiasis
  • Fungi tolerate higher glucose concentrations
  • UTI (especially if bladder emptying is impaired)
  • Periodontitis and dental caries
34
Q

Chronic Complication: Cataracts

A

Cataracts:

-Abnormal glucose metabolism because of accumulation of sorbitol and water lens or reduced transparency

35
Q

Chronic Complications: Pregnancy

A

Diabetes in mother may be exacerbated by:

  • Hormonal fluctuations
  • Metabolic changes

Increased incidence of spontaneous abortions and abnormalities

Infant birth weight is usually greater than average

Newborn predisposed to complications

Pathophysiology (9 decks)

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