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92 Cards in this Set

  • Front
  • Back
Hormones of the anterior pituitary

TSH

ACTH

FSH

LH

Prolactin

Growth Hormone

MSH

Endorphins

Thyroid

Adrenal Cortex

Testes, Ovaries

Testes, Ovaries

Mammary gland

Liver

Melanocytes in the skin

Opioid receptors

TSH

ACTH

FSH

LH

Prolactin

Growth Hormone

MSH

Endorphins

Thyroid

Adrenal Cortex

Testes, Ovaries

Testes, Ovaries

Mammary gland

Liver

Melanocytes in the skin

Opioid receptors

10% of cranial lesions

Most common prolactinoma

Present with visual changes due to pressure on optic chiasm

Treat with dopamine agonist and radiation
Growth hormone
Primarily promotes growth indirectly by stimulating liver’s production of somatomedins

Primary somatomedin is insulin-like growth factor (IGF-1)

Acts directly on bone and soft tissues to bring about most growth-promoting actions

Stimulates protein synthesis, cell division, and lengthening and thickening of bones

GH exerts metabolic effects not related to growth

Increases fatty acid levels in blood by enhancing breakdown of triglyceride fat stored in adipose tissue

Increases blood glucose levels by decreasing glucose uptake by muscles
Growth Hormone Deficiency

Due to pituitary defect or hypothalamic dysfunction

Laron syndrome, or Laron-type dwarfism, is an autosomal recessive disorder characterized by an insensitivity GH caused by a variant of the growth hormone receptor

Hyposecretion of GH in child is another cause of dwarfism

Symptoms: retarded skeletal growth, poorly developed musculature, excess subcutaneous fat
African Pygmies
African Pygmies

fails to respond to exogenous hormone in the presence of normal serum levels of growth hormone and of somatomedin ... Thus, the 'defect' appears to involve end-organ responsiveness to somatomedin
Acromegally

Pituitary secretes too much Growth Hormone

Due most common from Pituitary Adenoma secreting Growth hormone or rarely from tumors of other glands that secrete growth hormones

Epiphyseal Plates are closed so bones widen
Posterior Pituitary
Posterior Pituitary

Oxytocin –

stimulates uterine contractions,

milk ejection reflex in the mammary glands

Rise during sexual activity

ADH - antidiuretic hormone,

Released in response to electrolyte changes or fall in BP

stimulates retention of water action

blocked by alcohol and caffeine
Diabetes Insipides

Diabetes- “To pass through”

Polyuria, excessive thirst

Due to tumor, stroke, surgery, trauma, meds (lithium), hemochromosis, sarcoidosis, polycystic kidney disease, sickle cell anemia, destruction of thirst mechanism

Treatment with Vasopressin ( DDAVP in nasal spray or tablet form)
Parathyroid - what are the parts of it

4 compact glands located posterior aspect of the thyroid

Chief cells produce PTH

Oxyphil cells’ function is unknown
Function of the Parathyroid hormone
•Mobilization of calcium from bone: stimulate osteoclasts to reabsorb bone mineral, liberating calcium into blood.
•Enhancing absorption of calcium from the small intestine:. Parathyroid hormone indirectly stimulates the production of the active form of Vitamin D in the kidney. Vitamin D induces synthesis of a calcium-binding protein in intestinal epithelial cells that facilitates efficient absorption of calcium into blood.
•Suppression of calcium loss in urine: Prevents the excretion of calcium in the urine and stimulates loss of phosphate.
Hypoparathyroidism

Results in decreased of calcium and increased phosphorus in blood.

Leads to tetany and convulsions, and can be acutely life-threatening

Causes: surgical removal , autoimmune disorder, Hemochromatosis, Congenital absence, Magnesium Deficiency.

Treatment focuses on restoring normal blood calcium concentrations by calcium infusions, oral calcium supplements and vitamin D therapy.
Hyperparathyroid

Elevated serum calcium

Ademona

Sestamibi Scan - overactive parathyroid glands pick up agent faster than others

Minimally invasive surgery
Pseudohyperparathyroidiam

The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. I

Seen in:

Chronic Renal Failure where kidneys do not convert enough Vitamin D to the active form

Malabsorption- where vitamin D is not absorbed

Result:

Hypocalcemia

Hyperparathyroidism
Histology of the Thyroid
Follicular cells: responsible for secreting the thyroid hormones as well as thyroglobulin, a glycoprotein

Follicle contains Colloid
Thyroid hormones are stored extracellularly as part of the thyroglobulin which is the main component of the colloid

Parafollicular cells secrete calcitonin
Calcitonin

Produced by parafollicular cells of the thyroid

Acts to reduce calcium opposing the effects of parathyroid hormone

Decreasing Ca2+ absorption by the intestine

Decreasing osteoclast activity in the bones

Decreasing Ca2+ and phosphate reabsorption by the kidneys

Elevated blood calcium levels strongly stimulate calcitonin secretion, and secretion is suppressed when calcium concentration falls below normal.
Hypoparathyroidism

Results in decreased of calcium and increased phosphorus in blood.

Leads to tetany and convulsions, and can be acutely life-threatening

Causes: surgical removal , autoimmune disorder, Hemochromatosis, Congenital absence, Magnesium Deficiency.

Treatment focuses on restoring normal blood calcium concentrations by calcium infusions, oral calcium supplements and vitamin D therapy.
Thyroid Hormones

TSH

Free T4 – amount of active hormone which is available to enter the target organs.

T3- may be normal in hypothyroid, best for hyperthyroid

T3RU uptake- rarely ordered – measures the amount of thyroid binding hormone
Hyperparathyroid

Elevated serum calcium

Ademona

Sestamibi Scan - overactive parathyroid glands pick up agent faster than others

Minimally invasive surgery
Thyroid Antibodies
Thyroid Peroxidase Antibodies

TPOAB

Hashimoto and Graves

Thyroglobulin Antibodies

TGAB

Hashimoto and Cancer

Thyroid Stimulating Hormone Receptor Antibody

TRAB

Graves
Pseudohyperparathyroidiam

The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. I

Seen in:

Chronic Renal Failure where kidneys do not convert enough Vitamin D to the active form

Malabsorption- where vitamin D is not absorbed

Result:

Hypocalcemia

Hyperparathyroidism
thyroid effect on heart
Chronotropic
Increase number of β receptors
Inotropic
Enhance response to circulating catecholamines
Increase proportion of -myosin heavy chain (with higher ATPase activity).
Histology of the Thyroid
Follicular cells: responsible for secreting the thyroid hormones as well as thyroglobulin, a glycoprotein

Follicle contains Colloid
Thyroid hormones are stored extracellularly as part of the thyroglobulin which is the main component of the colloid

Parafollicular cells secrete calcitonin
thyrodMyxedema

is a skin and tissue disorder usually due to severe prolonged hypothyroidism

results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis

Also seen in Grave’s, Hyperthyroidism, Hoshimotos
Calcitonin

Produced by parafollicular cells of the thyroid

Acts to reduce calcium opposing the effects of parathyroid hormone

Decreasing Ca2+ absorption by the intestine

Decreasing osteoclast activity in the bones

Decreasing Ca2+ and phosphate reabsorption by the kidneys

Elevated blood calcium levels strongly stimulate calcitonin secretion, and secretion is suppressed when calcium concentration falls below normal.
Myxedema presentation

Skin thickening

Coarse skin

Change in facial appearance

Thickening nose

Swollen lips

Puffiness around the eyes

Jelly-like infiltrations in subcutaneous tissues

Slow speech

Mental dullness

Lethargy

Mental problems

Dry skin

Yellow skin

Swollen subcutaneous tissue

Weight gain

Thinning Hair

Brittle Hair

Bald Patches

Muscle Pain Deafness

Hearing Impairment

Carple tunnel syndrome

Constipation
Thyroid Hormones

TSH

Free T4 – amount of active hormone which is available to enter the target organs.

T3- may be normal in hypothyroid, best for hyperthyroid

T3RU uptake- rarely ordered – measures the amount of thyroid binding hormone
Thyroid Antibodies
Thyroid Peroxidase Antibodies

TPOAB

Hashimoto and Graves

Thyroglobulin Antibodies

TGAB

Hashimoto and Cancer

Thyroid Stimulating Hormone Receptor Antibody

TRAB

Graves
thyroid effect on heart
Chronotropic
Increase number of β receptors
Inotropic
Enhance response to circulating catecholamines
Increase proportion of -myosin heavy chain (with higher ATPase activity).
thyrodMyxedema

is a skin and tissue disorder usually due to severe prolonged hypothyroidism

results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis

Also seen in Grave’s, Hyperthyroidism, Hoshimotos
Myxedema presentation

Skin thickening

Coarse skin

Change in facial appearance

Thickening nose

Swollen lips

Puffiness around the eyes

Jelly-like infiltrations in subcutaneous tissues

Slow speech

Mental dullness

Lethargy

Mental problems

Dry skin

Yellow skin

Swollen subcutaneous tissue

Weight gain

Thinning Hair

Brittle Hair

Bald Patches

Muscle Pain Deafness

Hearing Impairment

Carple tunnel syndrome

Constipation
Cretinism
Severely stunted growth due to congenital hypothyroidism

Assoc with Iodine deficiency
Hashimoto

chronic lymphocytic thyroiditis
Hashimoto

chronic lymphocytic thyroiditis

an autoimmune disease where the body's own T-cells attack the cells of the thyroid.

It was the first disease to be recognized as an autoimmune disease.

Antibodies cause gradual destruction of follicles in the thyroid gland.
Hyperthyroidism and Thyrotoxicosis
Term for symptomatic hyperthyroidism

Hyperactivity,irritability, dysphoria, heat intolerance, sweating, anxiety palpitations, weight loss, diarrhea, tachycardia, atrial fibrillation, goiter

Very low TSH, high free T4
Graves Disease
Graves' disease is a thyroid-specific autoimmune disorder in which the body makes antibodies to the thyroid-stimulating hormone receptor (TSHR),

leading to hyperthyroidism

The autoantibodies produced in Graves' disease are not subject to negative feedback, so they continue to be produced and bind to TSHR even when thyroid hormone levels rise too high.

These antibodies act as agonists, stimulating more hormones to be released and thus leading to hyperthyroidism
Thyroid Storm
Thyroid storm is a crisis or life-threatening condition characterized by an exaggeration of the usual physiologic response seen in hyperthyroidism. Whereas hyperthyroidism can cause symptoms such as sweating, feeling hot, palpitations and weight loss - symptoms of thyroid storm are more severe, resulting in complications such as:

fever

rapid heart rate

nausea/vomiting

diarrhea

irregular heart beat

weakness

heart failure

confusion/disorientation

Fever tends to be one of the hallmarks of thyroid storm and can be as high as 105-106F. The actual diagnosis of thyroid storm is made on the basis of suspicion in patients with symptoms, and in the setting of elevated blood levels of thyroid hormones (T3 and T4
Pancrea s
ndocrine and exocrine organ

Endocrine organ: 1%

Islet cells – secretes

glucagon by alpha cells

Insulin by beta cells

Exocrine organ:Ascini

Buffers: controlled by secretin in duodenum

Enzymes:Controlled by CCK in intestines
Pancreatic Enzymes
Amylase which breaks down carbohydrates

Lipase breaks down fats

Proteases

Tripsin

Chymotrypsin

Carboxypeptidase
Pancreatitis
Blockage of excretory ducts by infection, ischemia or drugs ( alcohol )

Causes injury of the exocrine cells

Lysosomes in the damaged cells activate the surrounding pancreatic enzymes and digest surrounding cells

10-15% of patients the process does not stop and the pancreas is destroyed

Pancreaticpseudocyst – collection of enzymes, blood and necrotic tissues

Conservative treatment vs drainage
Diabetes Mellitus
Mellitum means HONEY

Diabetes is a group of Metabolic Disorders with the common manifestation: HYPERGLYCEMIA

Type 1 :insulin deficiency, autoimmune

Type 2 : insulin resistance, B cell defect

Gestational Diabetes

Polyuria, Polydipsea, Polyphagia
Risk Factors for DM
Obesity

Impaired Glucose Intolerance

Hypertension

Lack of Exercise

Poor diet

Gestational Diabetes

Smoking

Metabolic Syndrome
Who should be screened for DM
screening with fasting glucose or oral glucose tolerance test recommended for overweight patients > 45 years old (particularly with BMI > 25 kg/m2)

screening should also be considered in younger adults with

family history of diabetes

low HDL cholesterol

high blood pressure history of gestational diabetes or birth of baby weighing > 9 pounds

polycystic ovary syndrome (PCOS) or other clinical condition associated with insulin resistance (e.g., acanthosis nigricans)

habit of physical inactivity

vascular disease

ethnic group at increased risk (African-Americans, Native Americans, Hispanic Americans/Latinos, Asian American and Pacific Islanders)

recheck every 3 years if normal (fasting plasma glucose < 100 mg/dL [5.6 mmol/L] or 2-hour oral glucose tolerance test < 140 mg/dL [7.8 mmol/L]
Diabetic Ketoacidosis
Diabetic Ketoacidosis

In solution Ketone bodies dissociate releasing H ions threatening pH

Starvation increases ketones bodies as another form of fuel

Without insulin body cannot utilize insulin and body is in starvation mode

Type 1 and type 2 Diabetes

Treatment consists of hydration to lower the osmolality of the blood, replacement of lost electrolytes, insulin to force glucose and potassium into the cells, and eventually glucose simultaneously with insulin in order to correct other metabolic abnormalities, such as lowered blood potassium (hypokalemia) and elevated ketone levels. Many patients require admission to a step-down unit or an intensive care unit (ICU) so that vital signs, urine output, and blood tests can be monitored frequently. Brain edema is not rare, and so this may suggest intensive monitoring as well. In patients with severe alteration of mental status, intubation and mechanical ventilation may be required. Survival is dependent on how badly-deranged the metabolism is at presentation to a hospital, but the process is only occasionally fatal.


DKA occurs more commonly in type 1 diabetes because insulin deficiency is most severe, though it can occur in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. In a person known to have diabetes and being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis, the flu, or the development of a serious new health problem (e.g., bacterial infection, myocardial infarction).

DKA occurs more commonly in type 1 diabetes because insulin deficiency is most severe, though it can occur in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. In a person known to have diabetes and being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis, the flu, or the development of a serious new health problem (e.g., bacterial infection, myocardial infarction).
Usually in type 2 diabetics

Plasma glucose level of 600 mg/dL or greater

Effective serum osmolality of 320 mOsm/kg or greater

Profound dehydration (8-12 L) with elevated serum urea nitrogen (BUN)-to-creatinine ratio

Small ketonuria and absent-to-low ketonemia

Bicarbonate concentration greater than 15 mEq/L

Some alteration in consciousness

10 to 20% mortality

May be due to infection

Name change since Doma in < 10% of patients
Hypoglycemia
Insulin Reaction: inadequate food, exercise, first trimester of pregnancy due to fetus requirements, diabetic gastroparesis, insulin potientated by drugs: ethanol, salicylates, B- blockers

Hypoglycenic agent overdose

Autoimmune hypoglycemia

Pentamidine induced hypoglycemia- drugs lytic effect on B cells

Pancreatic B cell tumors- insulinoma- an insulin secreting tumor of the islets of langerhans
Adrenal Gland - what are it's two parts
Embedded above each kidney in a capsule of fat

Composed of two endocrine organs

Adrenal cortex

Outer portion

Secretes steroid hormones

Adrenal medulla

Inner portion

Secretes catecholamines
Adrenal cortex
Adrenal cortex

Consists of three layers or zones

Zona glomerulosa – outermost layer

Zona fasciculata – middle and largest portion

Zona reticularis – innermost zone

Categories of adrenal steroids

Mineralocorticoids

Mainly aldosterone

Influence mineral balance, specifically Na+ and K+ balance

Glucocorticoids

Primarily cortisol

Major role in glucose metabolism as well as in protein and lipid metabolism

Sex hormones

Identical or similar to those produced by gonads

Most abundant and physiologically important is dehydroepiandosterone (male “sex” hormone)
Aldosterone

Principal action site is on distal and collecting tubules of the kidney

Increases the reabsorption of sodium and water and the release (secretion) of potassium in the kidneys

Increases blood volume and as a result increases blood pressure

From zona glomerulosa- outer layer, mineralcorticoid

Aldosterone production is regulated partly by corticotropin (secreted by the pituitary gland) and partly through the renin-angiotensin-aldosterone system

Secretion is increased by

Activation of (RAAS) renin-angiotensin-aldosterone system by factors related to a reduction in Na+ and a fall in blood pressure

Direct stimulation of adrenal cortex by rise in plasma K+ concentration

drugs, such as spironolactone lower blood pressure by blocking the aldosterone receptor
Aldosterone Hypersecretion - May be caused by...
symptoms ..

May be caused by

Hypersecreting adrenal tumor made up of aldosterone-secreting cells

Primary hyperaldosteronism or Conn’s syndrome ( 75%)

Inappropriately high activity of the renin- angiotensin system

Secondary hyperaldosteronism

Symptoms

Excessive Na+ retention and K+ depletion

High blood pressure
Primary Aldosteronism
Primary Aldosteronism

Presentation: Hypokalemia and Hypertension

Assessment of renin – angiotensin system:

If normal or elevated in a person with no diuretics-no hyperaldosteronism

If low in presence of low K- check urine and serum aldosterone after starting NaCl suppliment- if suppression dx is made
endocrine effect of licorice
Eating large amounts of real licorice can produce all the symptoms of hyperaldosteronism. Real licorice contains a chemical that can act like aldosterone. However, most candy sold as licorice contains little or no real licorice.
Cortisol

Cortisol

is a glucocorticoid produced by the Zona fasciculata of the adrenal cortex

Stimulates hepatic gluconeogenesis (liver makes glucose)

Inhibits glucose uptake and use by many tissues, but not the brain

Stimulates protein degradation in many tissues, especially muscle

Increases Blood Pressure

Facilitates lipolysis

Plays key role in adaptation to stress
Sex Hormones
Secretes both male and female sex hormones in both sexes

Not high enough conc. to have any effect

Dehydroepiandrosterone (DHEA)

the most abundant androgen (male steroid hormone) secreted by the adrenal glands

Only adrenal sex hormone that has any biological importance

DHEA can also be converted into other steroid hormones, including testosterone and estrogen

DHEA levels decline with advancing age

Physiologically significant in females where it governs

Growth of pubic and axilla hair

Enhancement of pubertal growth spurt

Development and maintenance of female sex drive
Cushing Disease
Cortisol hypersecretion

Causes

Overstimulation of adrenal cortex by excessive amounts of CRH and ACTH

Adrenal tumors that uncontrollably secrete cortisol independent of ACTH

ACTH-secreting tumors located in places other than the pituitary

Signs and symptoms

Hyperglycemia and glucosuria (adrenal diabetes)

Abnormal fat distributions

“buffalo hump” and “moon face”
Diagnosis of Cushing Syndrome
either a Dexamethasone suppression test.(administration of dexamethasone and frequent determination of cortisol and ACTH level),

a 24-hour urinary measurement for cortisol offer equal detection rates

Recently cleared by the US FDA, is sampling cortisol in salive over 24 hours, which may be equally sensitive, as late night levels of salivary cortisol are high in Cushingoid patients
Adrenal Androgen Hypersecretion

Adrenogenital syndrome

Symptoms

Adult females

Hirsutism= male pattern hair growth

Deepening of voice, more muscular arms and legs

Breasts become smaller and menstruation may cease

Newborn females

Have male-type external genitalia

Prepubertal males

Precocious pseudopuberty

Adult males

Has no apparent effect
Adrenocortical Insufficiency

Primary adrenocortical insufficiency

Addison’s disease- all layers (zonas) undersecrete

Autoimmune disease

Aldosterone deficiency
»
Hyperkalemia (too much K+) and hyponatremia (too little Na+)

Cortisol deficiency
»
Poor response to stress
»
Hypoglycemia (low blood glucose)
»
Lack of permissive action for many metabolic activities

Secondary adrenocortical insufficiency

Occurs because of pituitary or hypothalamic abnormality

Only cortisol is deficient

Poor stress response, pigmentation of skin due to similarity with melanin
Addison’s Disease
Chronic Adrenal insufficiency

Etiology: autoimmune, infection, hemorrhage, metastatic disease , drug induced, (ketoconizole), sepsis, cortisol resistance, and X-linked adrenoleukodystrophy

Clinical Features:

Orthostatic hypotension

Weakness, anorexia, fatigue

Hyperpigmentation of the skin

Salt Craving

GI problemsAddison’s Disease
Acute Adrenal Crisis
People with Addison’s who are exposed to the stress of trauma, surgery or dehydration

Due to deficient cortisol

Can rapidly lead to death

Treatment: hydrocortisone sodium phosphate

Symptoms:

Hypotension

Shock

Dehydration

N/V and anorexia

Hypoglycemia

Weakness

Depressed mentation
Adrenal medula
Found in the center of the gland

Modified part of sympathetic nervous system

Chromaffin cells secrete catecholamines epinephrine and norepinephrine into the blood in response to body stressors

Epinephrine

Reinforces sympathetic system in mounting general systemic “fight-or-flight” responses

Maintenance of arterial blood pressure (vasostriction, increased CO)

Increases blood glucose and blood fatty acids
Stress Reaction
Pattern of reactions to a situation that threatens homeostasis

Stress

Generalized nonspecific response of body to any factor that overwhelms or threatens to overwhelm the body’s ability to maintain homeostasis

Stressor

Any noxious stimulus that brings about the stress response

Physical, emotional, chemical, infectious, social, physiological

All the actions are coordinated by the hypothalamus

Generalized stress response

Activation of sympathetic nervous system accompanied by epinephrine secretion

Prepares body for fight-or-flight response

Activation of CRH-ACTH-cortisol system

Helps body cope by mobilizing metabolic resources

Elevation of blood glucose and fatty acids

Decreased insulin and increased glucagon secretion

Maintenance of blood volume and blood pressure

Increased activity of renin-angiotensin-aldosterone system and increased vasopressin secretion
pheochromocytoma
A rare tumor that develops in the core of an adrenal gland.

Can develop at any age, but most commonly occurs in people between ages 30 and 60.

Increase catacolamines in the body

Symptoms

Rapid heart rate

Forceful heartbeat

Profound sweating

Chest pain

Upper abdominal pain

Severe brief headaches of sudden onset

Shaking (tremors) of your hands

Feeling of anxiety

Feeling of extreme fright

Pale skin
Anemia
Low RBC Count

Types:

Macrocytic MCV >100

Microcytic MCV < 80

Normocytic MCV between 80 and 100
Macrocytic Anemia

Also called Megaloblastic anemia

Large RBC

Due to B 12 or Folate deficiency

Seen in people with chronic Alcohol abuse
Pernicious Anemia

B 12 deficiency

B 12 usually absorbed by ileum when bound to intrinsic factor made by parietal cells

Shilling test tests for intrinsic factor

Due to gastritis, surgery or tapeworm

Tx: with B 12 injection
Microcytic Anemia

Small RBC

Lab:

MCV < 80

MCH < 27 pg

MCHC <32 g/dl

Anisocytosis

Poikilocytosis

Causes

Iron Deficiency

Sideroblastic Anemia

Thallessemia

Lead Poisoning
Iron Deficiency Anemia

Low iron in the body so Hgb cannot be formed

Low or normal reticulocyte count

20% female, 2 % male

Associated with blood loss and parasites

Pallor, Fatigue, hair loss, Pica

Lab:

Decreased ferritin
Thallassemia

Autosomal recessive blood disease

Major and Minor Classification

Reduced synthesis of one of the globin chains of hemoglobin

Alpha

Beta

Normal has 2 alpha chains and 2 beta chains

Lab

MCV is low

Target cells

Nucleated RBC

Anisocytosis

Poikiolcytosis
Normocytic Anemia

Decreased Hemoglobin and Hematocrit

Causes

Decreased Production

Increased Destruction

Increased Plasma volume
Increased RBC loss or destruction

Acute blood loss

Hypersplenism

Hemolytic disorders

Congenital conditions

Disorders of red blood cell membranes

Red blood cell enzyme deficiencies

Acquired conditions

Mechanical

Autoimmune

Paroxysmal nocturnal hemoglobinuria
Increased RBC loss or destruction

Acute blood loss

Hypersplenism

Hemolytic disorders

Congenital conditions

Disorders of red blood cell membranes

Red blood cell enzyme deficiencies

Acquired conditions

Mechanical

Autoimmune

Paroxysmal nocturnal hemoglobinuria
Decreased RBC Production
primary and secondary causes

Primary causes

Marrow hypoplasia or aplasia

Myelopathies

Myeloproliferative diseases

Pure red blood cell aplasia

Secondary causes

Chronic renal failure

Liver disease

Endocrine deficiency states

Anemia of chronic disease

Sideroblastic anemias
Anemia of Chronic Disease

“Anemia of Inflammation”

Seen with chronic illness

Perhaps a result of HEPCIDIN release in response to cytokines

Stops release of iron

Blunts RBC production

Produces more WBC

Lab

Low reticulocyte index

Normal or high ferritin

Normal TIBC
Sickle Cell Anemia
Abnormal sickle shape

Decreased movement depriving cells of oxygen

Vasoocclusive crisis causes ischemia and chromic pain

Prone to autoinfarction of spleen and infections

Osteomyelitis and leg ulcers
Hemolytic Anemia

Anemia secondary to RBC breakdown

RBC breakdown cause release of bilirubin then jaundice and dark urine. Also increased LDH.

Coombs test performed – looks for antibodies to RBC on the surface of the cell

Causes: autoimmune diseases, chronic diseases, drugs, Mechanical heart valves
Polycythemia Vera

Increased RBC due to bone marrow problem

Mean age 60

Asymptomatic to various symptoms such as generalized itch after warm water exposure

Erythromelolgia

Prone to blood clots

TX: blood letting
Aplastic Anemia

Bone marrow failure:

Multi lineage or Single lineage

Etiology: acquired or inherited

Radiation, chemicals, drugs, infections, autoimmune ( Marie Curie)

Presentation: infection, bleeding or anemia

Incidence: peak 20’s and fifth decade of life

Diagnosis: peripheral blood smear
Treatment of Aplastic Anemia

Immunosuppression

Immunostimulating

Antibiotics

Blood Transfusions risk of iron overload

Bone Marrow transplant- risk of host vs. graft reaction
*Death within 6 months without treatment
Leukemia

Cancer of the blood cells or bone marrow causing and elevation in the WBC count

Divided into Acute or Chronic and Lymphocytic or Myelogenous Leukemias
Acute vs Chronic Leukemia

Acute leukemia

characterized by the rapid increase of immature blood cells.

crowding makes the bone marrow unable to produce healthy blood cells

occurs in children and young adults.

Immediate treatment is required in acute leukemias due to the rapid progression and accumulation of the malignant cells, which then spill over into the bloodstream and spread to other organs of the body.

-------------------------

Chronic leukemia

distinguished by the excessive build up of relatively mature, but still abnormal, blood cells.

Takes months or years to progress, the cells are produced at a much higher rate than normal cells, resulting in many abnormal white blood cells in the blood.

occurs in older people, but can theoretically occur in any age group.

Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy
Acute Lymphoblastic Leukemia
( more commonly -a disease of children)

Excess Lymphoblast – overproduction of immature WBC

Peak age 2 to 5, another peak in older

Cure 85% children 50% adults

Worse as patient gets older

Presence of Philadelphia Chromosome- poor prognosis

Treatment- radiation, chemo, bone marrow transplant
Chronic Lymphocytic Leukemia

Most common type of leukemia

Patients > 50, occasional children, M>F

Results from the accumulation of Mature B cells or rarely T cells

Stages 0 to 4 with survival in years

0 only Lymphocytosis > 15

I with lymphadema 8

II with splenomegaly 6

III with anemia 3

IV with thrombocytosis 2
Acute Myelogenous Leukemia

Cancer of the myeloid lines- which give rise to granulocytes, monocytes, RBC and platelets

Auer rods are pathneumonic

Most common leukemia in adults

Five-year survival varies from 15–70%

Presentation – flu like symptoms

Some experience swelling of the gums because of infiltration of leukemic cells into the gum tissue.

Rarely, development of a solid leukemic mass or tumor outside of the bone marrow, called a chloroma
Chronic Myelogenous Leukemia

Hall mark is Philadelphia Chromosome

Presentation: Elevated WBC on routine CBC and splenomegaly with fatigue, occasional platelet elevation.

Blast Crisis -final phase in the evolution of CML – 30 to 40 % of blasts in bone marrow

TX: chemotherapy
Hairy Cell Leukemia

Mature B cell neoplasm

Cells look “Hairy” in lab

2% of all leukemias mostly men> 50

Easily goes into remission

Great chance of developing second cancer
Lymphoma

Tumors develop in the Lymph Nodes

Types:

Hodgkins with 5 sub groups

Non- hodgkins with 20 subgroups
Hodgkins Lymphoma

1% of all cancers

Starts in 1 lymph node and spreads to others

Biopsy shows Reed Sternberg cell

2 age groups: 15 to 35 and > 55

Etiology ?? Some consider a viral etiology

98% survival in early stages goes down to 80% in late stages

Symptoms: Night Sweat, pains, fever, enlarged LN, hepatospleenomegally.
Multiple Myeloma

Malignant proliferation of plasma cells

Most common bone cancer in adults

30% dx as incidental finding on x-ray

Median Survival 3 years

Characteristics:

Calcium elevation

Renal Failure: Bence Jones Proteins in the Urine

Anemia

Bone Lesions

Bone pain esp. sternum and skull, ribs and back
Urticaria

Multiple etiologies

Food and additives

Drugs

Infections

Inhaled Allergens

Internal Disease

Due to physical exposures – cold, heat
Barrett’s Esophagus
Squamous cells of esophagus become columnar cells with intestional characteristics

Develops into adenocarcenoma

EGD q 2 years with biopsy
Esophageal Varices

Esophageal varices develop when normal blood flow to your liver is blocked. The blood then backs up into smaller, more fragile blood vessels in your esophagus

Mortality rate- 50%

Treatment-

Hemodynamic care

Band ligation

Sclerotherapy

Somatostatin or Octreotide

Vasopressin
Stages of Renal Disease

Stage 1 CKD

Slightly diminished function; Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies

Stage 2 CKD

Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.

Stage 3 CKD

Moderate reduction in GFR (30-59 mL/min/1.73 m2)

Stage 4 CKD

Severe reduction in GFR (15-29 mL/min/1.73 m2)

Stage 5 CKD

Established kidney failure (GFR <15 mL/min/1.73 m2,) Dialysis

Causes

The most common causes of CKD are DM, HTN, glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.