1

ENDOCRINE
PITUITAIRY
Anterior (glandular)
- FSH & LH – stimulate of maturation of testicles and ovaries
- GH – works primarily on bone and muscles
- Prolactin – stim milk production
- ACTH – adrenal cortex – cortisol-based hormones; messenger hormone
- TSH – messenger; stim T3 and T4 (elevated levels mean hypothyroidism)
Posterior (storage)
- ADH – tells your kidneys how much water to conserve (diuretic)
- Oxytocin – mammary glands; smooth muscle in the uterus
o In males it induces sexual arousal
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MECHANISMS OF HORMONAL ALTERATIONS–

- Hypo or hyper secretion
- Failure to send signals (feedback system)
- Break down before they reach desired target or destroyed by antibodies
- Inadequate blood supply to gland
- Ectopic sources of hormone production  elevated levels
- Defective receptors or decrease in number
- Failure of secondary messenger system
o Most hormones need a secondary messenger to function
- Very easy to infarct the gland because of anatomy
o Problem with the stalk

POSTERIOR PITUITARY

Syndrome of inappropriate antidiuretic hormone (SIADH)

- Hyper secretion of ADH from ectopic tissue (tumor of the duodenum,
stomach, pancreas, bladder)
- Can be due to cancer or transient post-op condition
- Pulmonary disease > ADH > infected lung tissue and brain damage
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- May be caused by medications taken by the elderly such as hypoglycemic

drugs, general anesthetics, NSAIDS
- Clinical manifestations are related to enhanced renal water retention
o Water follow sodium and higher concentration
- Hyponatremia > seizures, confusion, lethargy, muscle twitching, convulsions
- Hypoosmolality, water toxicity > Brain damage
- Treat by correcting hyponatremia w. hypertonic saline and fluid control
- XS fluid reduces renin production which decreases aldosterone > worsens
this condition
o Need renin to help kidney release water
- Vasopressin – ADH receptor antagonist
- Sodium excretion is normal

Diabetes Insipidus
- ADH deficiency
- Polyuria and polydipsia
- Increased plasma osmolality
o Concentration (^ in osmolality > ^ concentration)
- Partial or total inability to concentrate the urine
- Neurogenic
o Insufficient secretion of ADH
o Any organic lesion of the hypothalamus, pituitary stalk, or posterior
pituitary
o brain lesion, stroke, thrombi
- Nephrogenic
o Normal amount of ADH in the blood
o Inadequate response to ADH in renal tubules
o renal tubules do not respond due to damage like pyelonephritis or
polycystic disease > permanent damage
- Kidneys produce 47 gallons a day diabetes insipidus = 12 gallons

Hypopituitarism – absence of one or more anterior pituitary hormones or complete

failure
- Damage to stalk
- Infarction
- Lesions like an adenoma
- TBI (traumatic brain injury)
- Meningitis
- Effects depend on which hormone is affected
o Sometimes all, sometimes one
- Panhypopituitarism – whole gland is affected
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Hyperpituitarism
- Adenomas are usually benign, slow growing and usually involve the ant.
Pituitary
o Headaches, seizures, blindness
o Optic chiasm is right behind the pituitary, so if there is tumor it will be
compressed = blindness

Growth Hormone
- Giantism: hypersecretion of growth hormone in children: taller you get;
harder your hearts working because plate is open
- Acromegaly – plate is closed after puberty

Acromegaly
- Bony overgrowth and organ overgrowth
o Collagen is laid down first
o Increased pressure on organ
- Metabolic signs – increased fat breakdown and decrease glucose uptake >
insulin resistance > glucose intolerance
- Increase in glucose > hyperinsulinism > decreased sensitivity > Diabetes
- Increased risk for colon cancer
- Increase growth of CT
- Enlarged tongue, active sweat gland and sebaceous glands
- Bony enlargements of the hands, vertebrae, face, feet > nerve entrapment >
nerve damage > weakness, muscular atrophy, and sensory changes in the
hands
- Extra bone development (osteophytes)
- Mandible grows first and back teeth will clamp together making it difficult to
close front teeth
- Cardiomyopathy > organ growth > hypertension > left ventricular heart
failure

Prolactinoma
- Pituitary hormone that secretes prolactin
- Most common hormonal active pituitary tumor
- Prolactin secretion can also be caused by renal failure, PCOS, primary
hypothyroidism, and breast stimulation
- Estrogen and anti-depressants can cause it as well
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Hypothyroidism
- Congenital or acquired
- Goiter - TSH is trying to get thyroid to make more T3 T4, and it is in
overdrive but not producing > hypertrophy > goiter
- Lab tests – TSH levels elevated
- Myxedema – sign of chronic hypothyroidism; large amounts of proteins and
mucopolysaccharides bind water > boggy edema
- Effects the hands the feet, the eyes, tongue thickens, affecting speech >
may lead to coma
- Hypothermia, hypotension, hypoventilation, hypoglycemia
- Treat with thyroid supplement
- HASHIMOTOS THYROIDITIS – most common cause of hypo; autoantibodies;
autoimmune attacks the thyroid gland and begins to destroy it
o Antithyroglobulin AB > tissue destruction

Hyperthyroidism- also called thyrotoxicosis

- Grave’s disease: #1 cause for hyper (autoimmune)
o Make autoantibodies that bind to the thyroid gland that the thyroid
sees as TSH
 Imposter
o Have to remove thyroid if can’t get under control
o TSI thyroid stimulating autoantibodies
- Low levels of TSH
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- Goiter - over production of T3 & T4, trying to keep up with demand >
hypertrophy
- Radioiodine thyroid Uptake scan
o Need iodine to make T3 T4
- Exophthalmos – bulging eyes; inflammation and periorbital edema, blurred
vision
- TX meds that block t3 t4 synthesis and beta blockers

Nodular Thyroid disease

- Follicular cells function autonomously and produce TH
- Some follicular cells shut down
- Increased colloid > follicles get bigger. Not enough iodine to produce t3 t4
- Can lead to hyperthyroidism
o You can have a nodule that is a benign growth
o Cells actually get large waiting for iodine (idk look this up)

Thyroid Storm
- Undiagnosed cases of Graves and they are subjected to stress like an
infection, pulmonary or cardiovascular problems, trauma, seizures, surgery
- Excess T3 T4 exceeding metabolic demands
- High fever, tachycardia, CHF, CNS signs like restlessness
- Life threatening often fatal
- Treatment: drugs that block T4 synthesis, beta blockers (slow heart rate),
steroids, and iodine

Subclinical thyroid disease

- TSH levels out of normal limits while T3 and T4 levels are normal
- No evidence that providing treatment benefits the patient

Thyroid Cancer
- #1 endocrine cancer
- TH levels normal
- Papillary follicular and medullary (in order of aggression low to high)
o Medullary is the worst and tends to metastasize
- S&S
o Usually have normal levels of T3 T4
o Tumors usually don’t produce T3 T4 but they can
o Usually no symptoms

Parathyroid Disorders
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- PTH job is to increase calcium levels in the blood

- Hypoparathyroidism
o Abnormally low PTH levels
o Usually from surgery where thyroid is taken out and para- is not intact
o May be due to hypomagnesium due to alcoholism, malnutrition,
malabsorption of Mg
 Need magnesium to produce PTH
 Increase muscle spasms, convulsions, laryngeal spasms, dry
skin, hair loss,
 Treat w. Vit. D and calcium supplement
- Hyperparathyroidism
o Primary – gland is malfunctioning
 Excess secretion of PTH from one or more para glands due to
adenoma
 Osteopenia, kyphosis, hypercaluria, alkaline urine due to
increase in phosphate hypophosphaturia > kidney stones;
decreased response to ADH; nausea, vomiting
o Secondary
 Increase in PTH secondary to a chronic hypocalcemia due to
renal disease w. decreased activation of Vit. D or mal absorb of
calcium

Adrenal Gland
- Androgens, mineralocorticoids, aldosterone
- Glucocorticoids
o Increases glucose concentration in blood stream
o Need glucose for energy in times of stress or when glucose is low
- ACTH – diurnal patterns
o Messenger hormone
o Constantly producing all day or night
o Make sure you are ready to face the next crisis (emotional or
physical)
- Hepatic gluconeogenesis
o Cortisol stimulates the release of glucose from the liver
o Break down all the glycogen you have and make glucose
- Taking cortisone supplements (suppresses immune response)
- Taking topical cortisol thins the skin because it interferes with collagen
production
o End up with osteoporosis
o Increases heart rate, vasoconstriction
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Addison’s Disease
- Need to “add in” a little ACTH - Cortical hormones low
- Primary adrenal insufficiency
- Autoimmune destruction is the most common cause
- 90% destroyed before S&S manifest
o Cortisol reduces inflammation
- Hormone Therapy forever
- Infection can cause low ACTH levels as well
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Cushing’s Disease
- Have a cushion of cortisol – excess ACTH
- Osteoporosis – destruction of bone proteins
- HTN
- Hypokalemia and hypernatremia: release a ton of Potassium but retain water
and sodium
o aldosterone
- Gluconeogenesis, insulin resistance
o Lets make tons of glucose! Producing tons of insulin to tuck away
glucose in the cells
- Increase in gastric acid secretion
- Increase in androgens
o Too much cortisol > androgens
- Treatment: surgery, drugs that block steroid synthesis
- Buffalo Hump – accumulation of fat on back of neck; superclavicular fat
pads
- Moon Face – round face
o Can be on treatment with cortisol will cause this as well
o Fluid accumulating in the face
- Stretch marks because not enough collagen
o Collagen holds the skin up
- Hirsutism – facial hair
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Diabetes Mellitus
- #1 predisposing factor for type 1 is obesity
- Insulin – promotes glucose uptake, inhibits gluconeogenesis, prevents fat
breakdown, Increases protein synthesis
- Glucagon – produced by the adrenal gland. Glycogenolysis – breaks down
glycogen to glucose; this is a problem because we already have too much
glucose
- Amylin - works with insulin; suppresses postprandial secretion of glucagon,
job is to help reduce glucose levels
- Somatostatin – delta cells; release is inhibited by insulin; holds back food in
stomach to increase absorption time; release is inhibited by insulin

Type 1 Diabetes:
- Used to call type 1 juvenile, insulin dependent = lose the ability to produce
insulin
- Year 1-9 destroying beta cells in pancreas slowly.
- Can get down to 20% functioning cells before we notice any symptoms
- Test urine and + glucose
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- Beta cells are shot and they are insulin dependent > pump
- Given a shot/pump b.c insulin breaks down in the GI tract
- Considered autoimmune so not necessarily a juvenile disease
o Autoantibodies against insulin or beta cells

Type 2 Diabetes
- Insulin resistant
- Beta cells are fine
- Glucose opens cell door to allow ATP production
- Pancreas functions
- Starving in the land of plenty = plenty of glucose but the cells are starving
and they can’t let glucose in.
- Next step would be to break down fat to try and make ATP, but we still cant
get glucose into the cell so there is an abundance of glucose.
- Intraabdominal fat >
- 3 cardinal (initial) signs: polyuria, polydipsia, polyphagia (both T1 and T2)
- Urinate out the excess glucose > trying to dilute urine
- Hyperglycemia
- Increase in leptin and decrease in adiponectin causing an increase in
inflammation and decrease in insulin sensitivity
o Adiponectin enhances insulin

Gestational diabetes: diabetes developed during pregnancy and is gone after

pregnancy
- But can increase risk for diabetes down the road
- Large babies also increase risk

Risk Factors:
- Family history
- African American, native American, Asian American, pacific islander
- Htn
- PCOS – develop hyperinsulinemia
- Lack of physical activity
- Baby delivered over 9 lbs and had gestational diabetes

Metabolic Syndrome: predisposes you to diabetes

- Obesity
- High triglycerides and low HDL’s - hyperlipidemia
- HTN
- Elevated CRP (inflammatory compound)
- Insulin resistance
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- Malfunction of vascular endothelium > leads to abnormal fibrinolysis (clot

breakdown): increases in plasminogen activator inhibitor
- Macrovascular disease – coronary and cerebral vessels, peripheral arterial
disease
- 5 SIGNS in including elevated fasting blood sugar, must have 3 of the 5

Drugs that may cause hyperglycemia:

- Diuretics > K drop > drop in insulin release
- Glucocorticoids – body is getting ready for next crisis
- Oral contraceptives
- Antipsychotic agents

S&S:
- Polyuria: trying to get rid of EX glucose
- Polydipsia: ADH levels down, thirsty
- Polyphagia: hungry all the time, cells want glucose bc glucose can’t get into
the cell
- Weight loss: burning fat
- Blurred vision: polyol pathway – not every cell is dependent on insulin for
glucose absorption: nerves, RBCs, retina

Advanced glycosylated end products (AGE) – glucose is stuck to stuff

- Draws water into RBC making it swollen and stiff
o Microcirculation (capillaries) compromised; swollen sticky RBC does
not bend to fit through capillary they get stuck
 Not selective: brain, glomerulus, heart etc.
o Amputation because circulation is lost b.c blood flow is blocked
- Increased vascular permeability
- Nerves become more permeable
o Glucose will enter cells that don’t need insulin key ie: nerves =
diabetic neuropathy
 Water moves in
o Retinal cells: glucose enters > sorbitol
 Water moves into retinal and swells it up
 Breaking down mitochondria, sodium potassium pump > cells
die> blindness
 Glucose moves to cells that will allow it to enter
- Increased arterial stiffness due to cross linking of glucose to proteins in the
vessel wall; thickened basement membrane: thickened vessel
o Leads to HTN, increased risk of clots, do not have the ability to break
down the clots
o Endothelium damaged = no nitric oxide production = no vasodilation
- Binding cells including macrophage, endothelial, and induce the secretion
of cytokines > release CRP
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- Advanced sign is protein in the urine because damage to the glomeruli

- bacteria LOVE glucose so higher risk for infection
o Immune compromised
o Can’t give antibiotics b.c circulation is plugged up so can’t get
medication to the problem

Diagnostic Tests:
- Should test after age 45 for sooner if there is a family history
- A1C: should be 7 or less
o glucose sticks to hemoglobin
- FBS – fasting (12 hour fast)
o Most accurate
- Glucose tolerance test (gtt): around the 100mL mark or below
o more accurate (sugar solution test in 2 hours, should be low and
stored away inside cells) (pregnancy test routinely)
- Urine test – can do from home

Treatment:
- Diet
- Exercise (weight loss improves lipid profiles)
- Meds:
o Metformin – inhibits the formation of glucose by the liver and makes
peripheral tissue more sensitive to insulin (more keys and more locks
to open the door).
o Insulin – injected as it is broken down by the GI tract

Diabetic Ketoacidosis:
- Excess of glucose but cells cannot get to it > breakdown of fat > fatty acids
and ketone acids > drop in pH > metabolic acidosis
o Often preceded by vomiting and polyuria and polydipsia;
hyperglycemia, acidosis, ketonuria
o Diabetic coma due to ketoacidosis
o Leads to Kussmaul respiration
- Insulin deficiency and glucagon excess
- Often preceded by emotional or physical stress
- Hypoglycemia – insulin shock

Simonyi Effect– insulin induced hypoglycemia produces a rebound hyperglycemia

due to release of glucagon, cortisol and growth hormone
- Dawn Phenomena– elevated glucose between 5-9 AM
o Increase in glucagon > gluconeogenesis
o Decrease in activity
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o Evening snacking
o Insufficient evening dose of insulin
o Increase in cortisol and growth hormones overnight

Chronic complications:
- Delayed gastric emptying
- Nephropathy: leading cause of kidney disease; glomerulosclerosis;
proteinuria; ESRD (end stage renal disease)
- Neuropathy: nerve damage/inflammation (very painful)
- Retinopathies: blindness
- Macrovascular disorders: CAD, PVD, CVD
- Foot ulcers: loss of sensation/circulation
- Impaired wound healing – poor circulation
- Gangrene due to PVD
- Immunocompromised
- 2x likely to suffer from a stroke with type 1 &2
- MIs, CHF, and ESRF

CHAPTER 21 ALTERATIONS OF
HEMATOLOGIC FUNCTIONS
Anemia – reduced ability for the blood to transport oxygen
- Causes:
o Impaired erythrocyte production
o RBC’s don’t live as long
o Blood loss; hemorrhage (acute or chronic)
o Increased erythrocyte destruction
o Less Hb
o Defective Hb
o Lack of oxygen in the room (in the mountains O2 in lower %)
- Chronic anemia and volume loss > interstitial fluid will move into the blood
vessel
- Acute onset (hemorrhage) the body will vasoconstrict as a normal response
shunting blood to vital organs and activate RAA (severe)
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- Morphology
o -chromic: hemoglobin content
o -cytic: size

- S&S:
o Reduced oxygen-carrying capacity of blood > tissue hypoxia
o Fatigue and weakness
o Dyspnea
o Ventricular hypertrophy
 Need to know why (severe)
o Pallor (lips, nail beds, skin, conjunctiva)
o Koilonychia due to hypoxia seen with heart problems
o Finger clubbing due to chronic lack of oxygen
- Tests:
o CBC

Megaloblastic anemia or macrocytic normochromic anemia

- Large RBC’s
- Normal hemoglobin (normochromic)
- Commonly caused by vitamin b12 or folic acid deficiency
o Caused by impaired DNA synthesis leading to enlarged RBCs
o Vitamin B is needed to complete DNA processing. The cells will
continue to grow as they are waiting for the DNA to close up shop.
Will see enlargement it on blood smear. Cells will die prematurely
leading to anemia because they do not mature correctly and need
DNA for function
o Slowly develop – overproduction of Hb during prolonged cell cycle.
Can accumulate more Hb and make the cell appear larger

Pernicious Anemia
- Most common type of macrocytic anemia
- Caused by vitamin b12 deficiency
- Often associated with autoimmune gastritis, gastric bypass, and PPI’s
- Pernicious = highly injurious or destructive. Used to be fatal
- Absence of intrinsic factor (transporter required for gastric absorption of
b12) essential for maturation and DNA synthesis of red blood cells
- Congenital or autoimmune
- Usually part of polyendocrinopathy (multiple endocrine organs)
o Hashimoto thyroiditis, Type 1 Diabetes, Addison Disease, Grave’s
Disease and Myasthenia Gravis
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- Chronic gastritis > gastric atrophy > auto antibodies against gastric H+, K+,
ATPase > deficiency of all gastric secretions in stomach (hydrochloric acid,
pepsin, and IF) > malabsorption of b12

- S&S:
o anything associated with poor oxygenation.
o neurologic problems from nerve demyelination. Spinal cord
degeneration > loss of position and vibration sense, ataxia and
spasticity > not reversible

- Treatment: injection of Vitamin B12 because if you eat B12 you will still not
have intrinsic factor to absorb it.

Folate Deficiency Anemia (folic acid):

- Only get from diet
- Need from RNA and DNA synthesis
- Increased amounts are required during pregnancy and breast feeding
- Absorbed in the upper small intestine and does not require any other
element to facilitate absorption
- After absorption, stored in the liver
- Occurs more often than b12 particularly in alcoholics and people who are
chronically malnourished
- S&S: cheilosis (scales and fissures in mouth), stomatitis (inflammation of
the mouth), painful ulcerations of the buccal mucosa and tongue,
dysphagia, flatulence and watery diarrhea
- Can be caused by undiagnosed Chron Disease or UC

Iron Deficiency Anemia (IDA)

- Most common type of anemia
- Inadequate dietary intake or chronic blood loss OR BOTH
- Deplete iron stores; need iron to make hemoglobin
- Stomach produces hydrochloric acid to absorb iron
- In developed countries due to pregnancy and continuous loss of blood
- 2 – 4 mL blood loss (1 – 2 mg iron) enough to cause IDA
- Menorrhagia (excessive menstrual bleeding) causes IDA in females
- Ulcers, hiatal hernia, esophageal varices, cirrhosis, hemorrhoids, UC, or
cancer
- NSAIDS, surgical procedures that decrease stomach acidity/transit time
(gastric bypass), insufficient intake of dietary iron,
- S&S:
o early symptoms vague: weakness, fatigue etc.
o LATE SIGNS:
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 structural and functional changes in epithelial tissue.

Fingernails are brittle and spoon shaped.
 Tongue papillae atrophy and causes soreness, redness,
burning (glossitis)
 Angular stomatitis (dry, cracked corners of mouth)
 Difficulty swallowing due to web of mucous and inflammatory
cells at the opening of the esophagus > could become
cancerous
 Pica: physical sign of anemia. Usually associated with Fe
deficiency the pt habits change and does nothing to change
the anemia. The person will crave it
 Eating dirt, clay, newspaper, kitty litter
 Test ferratin because stored iron is different
- Treatment:
o Iron pills
o Antibiotics

Normocytic-Normochromic Anemias Table 21-2 – reduction in count but normal

size and hemoglobin content

- Aplastic anemia: radiation and chemicals suppress hematopoiesis; usually

autoimmune causes
o WBC production is reduced/affected; can be due to treatment or
autoimmune
 RBC and WBC are affected in the bone marrow
o 2/3 cases are idiopathic
o EPO stimulates bone marrow to produce RBC’s

- Post Hemorrhagic Anemia – caused by sudden blood loss

- Hemolytic Anemia – RBC’s are broken down and don’t last long
o Acquired from infections or drug use
o Chronic inflammation
o AIDS can bring RBC count down

Sickle Cell Anemia

- Inherited and hemoglobin deficit; acidosis and oxygen affinity
- If you have two recessive genes you will get it
- Get one recessive gene 50% of cells will be affected > basically normal
life. 2 recessive genes > 100% of cells are affected > more susceptible
to malaria
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- Oxygen and drop in pH

- Sickle cell will have one portion of the chain change loosing repulsion
(negative charges)  hemoglobin cannot keep 3D shape and flatten 
can lead to occlusion of capillaries  sickle cell crisis – leads to
thrombotic issue where a lot of capillaries are occluded; very
painful/discomfort
- S&S:
- Thrombotic crisis = sickle cell crisis
- Pain
- Discomfort
- Weakness
- Treatment:
- Avoid oxygen deficiency
 As they reoxygenate is where the problem occurs
- They do not do bone marrow transplants anymore
- Usually lifestyle changes

Polycythemia Vera
- Too much of everything: WBC’s, RBC’s, and platelets
- Bone marrow is in hyperdrive making RBC’s; don’t know why
- Leads to thick blood > slows blood flow > clots, strokes, MI

- Primary – from birth; bone marrow is producing too much

- Secondary – excess EPO due to medication and stimulates bone marrow

into hyperdrive
- May be a kidney problem
- Typically do not know the cause

- S&S:
- water makes them itch
- HA
- Dizziness
- Hearing and vision loss
- Increased blood pressure > vasodilation > Pink/red face

- Treatment:
- Phlebotomy – take blood out
- Myelosuppressive drugs – slows down bone marrow

White cell disorders:

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Leukopenia
- Low WBC count
- Viral infection

Leukocytosis
- High WBC count
- Bacterial Infection

Neutropenia
- Higher risk of infection
- First on site; low count = risk for infection more so than WBC’s

Alloimmune neonatal neutropenia

- Born with less neutrophils than they should because mother’s neutrophils
were attacking theirs
- Mom and baby blood cross in amniotic sac and neutrophils are
destroyed by mother. Baby’s MCH complex is half mom and half Dad.
Bone with less neutrophils; baby can rebound unless there is a bone
marrow issue.
- can be a sign of cancer

Infectious Mononucleosis
- acute infection of B lymphocytes
- caused by EBV (Epstein Barr Virus) or cytomegalovirus (CMV)
- increase in number of cells that only have a single nucleus (B-cells
primarily)

Transmission:
- Saliva mostly
- Rectum, genitals, and respiratory tract

S&S:
- Start to show symptoms at the point of contact
- Early flu like symptoms
- Fever, sore throat (pharyngitis), cervical lymph node enlargement &
fatigue
- Splenomegaly – busy working on B cells > enlargement

Tests:
- Monospot

Treatments:
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- Antibiotics do not help

- Viral > run its course
- Problem is that it can be hard to beat > liver inflammation

Leukemia:
- Cancer of bone marrow and lymph nodes but not always blood
- Leukemia: uncontrolled proliferation of malignant leukocytes >
overcrowding of bone marrow > inability to produce other cells
(Neutrophils, Basophils, Lymphocytes etc.)
- Lymphoma is common post cardiac transplant due to
immunosuppressant drugs
- Radiation/X-rays increase risk for cancer and down syndrome
- Only overproduce B cells that are not effective
- B cells produce antibodies

Acute –
- Abrupt onset; without treatment = fatal
- Undifferentiated/immature blast cells
- Acute lymphocytic Leukemia (ALL) – common in kids; more fatal in adults
than kids. In adults, B & T cells are affected > risk for infection stronger
- Acute myelogenous leukemia (AML) – found in bone marrow (myeloid
tissue)

Chronic –
- Chronic myelogenous leukemia (CML) – found in bone marrow without
short onset.
- Philadelphia Chromosome translocation in 95% of cases
- Can develop spontaneously
- Better differentiation of cells, but the still don’t work properly
- Better chances of treatment
- Chronic Lymphocytic Leukemia (CLL) – producing defective lymphocytes
- They never die; no apoptosis

- Overproducing of WBC’s
- B cells are defective and too many are produced
- Usually platelet deficient
- Chronic is better than acute
- Slow growing > better chance to treat because body can adapt
- If levels of WBC’s are sky high usually cancer

- S&S:
- Fatigue & sick all the time
- Lymphadenopathy (enlarged lymph nodes)
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- Headache
- Bleeding gums

- Treatment:
- Car T cell therapy
- Lymphoma and leukemia treatment

Malignant Lymphoma – Hodgkin and Non-Hodgkin

- Hodgkin
- Enlarged lymph nodes
- Reed Sternberg (RS cells) present; used to diagnose, but can be
present in other diseases
- Can spread to other nodes
- Adult form can usually be cured if diagnosed early

- S&S:
- Painless lymph adenopathy
- Cervical chains swell; not single node swelling
- Night sweats
- Weight loss
- Mass in the back of neck
- Axillary nodes enlarged
- Inguinal nodes enlarged
- Popliteal node enlarged

- Treatment:
- Chemo
- Radiation
- Surgery
- Cart T cell therapy

Non-Hodgkin
- group of disorders
- Includes NK, T & B cells
- Lack RS cells
- Starts in lymph nodes and spreads to other lymphatic tissue
- Immunocompromised at greater risk (HIV)
- Not a chain; can pop up anywhere & be widespread

- Tests: Pet scan

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Multiple Myeloma
- Bone marrow disorder
- Malignant plasma cells (b cells) proliferation and osteolytic lesion with
bone marrow infiltration
- Bone most effected: vertebrae, ribs, skull, pelvis
- Eats away at bone

- Tests:
- Bence Jones proteins present in urine > damage to renal tubules
- M protein most prominent protein in blood > diminished or absent
antibodies
- Contributes to many clinical manifestations of disease

- S&S:
- Bone pain
- Rarely occurs before 40
- Kidney damage > Renal failure
- Hyperphosphatemia – hole in the bone
- Calcinuria
- Hypercalcemia
- Anemia
- Punched out lesion of skull
- Pneumonia
- Pyelonephritis

- Treatment:
- Bone marrow transplant

Thrombocytopenia
- Thrombocytosis- elevated platelet count
- Thrombocytopenia – reduced platelet count due to bone marrow
malfunction

- Causes:
- Leukemia
- HIV
- Chronic renal failure (splenic sequestered or pooling)
- Drugs (quinine-based drugs and heparin)
- Purpura – leaking blood vessels > blood accumulates in the skin
- Petechiae – spots due to broken capillaries

Impaired Platelet Function

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- May be inherited or acquired due to NSAID’s or ASA use because it

interferes with platelet aggregation
- Liver Disease
- Vitamin K deficiency

Disseminated Intravascular Coagulation (DIC)

- Spread out intravascular coagulation
- Idiopathic > clotting all over
- No bleeding > release tissue factor > but blood clots
- Form multiple clots
- Leads to necrosis
- Often post-partum
- Can kill you
- Additional bleeding occurs and hemorrhage

CHAPTER 5
Body water men have more because of higher body mass
Water is charged – ionic
Adipose holds less water

Body water
- 33% extracellular
o 25% interstitial
o 8% plasma
- 66% intracellular

Hydrostatic pressure- pressure created from blood inside the vessels

Oncotic pressure – albumin draws stuff in
- Albumin should always be inside vessel
- Why oncotic pressure does not change

Edema
- Accumulation of fluid between the cells (interstitial fluid)
- Increased CFP
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- Decreased CCP
- Increased capillary permeability
- Lymphatic obstruction: one way valves: pick up excess fluid
- Anasarca – generalized body edema

- S&S: depends on where the swelling is for example vocal cords or lungs
o May be localized or generalized
o Usually happens first in the feet – gravity
- Lymphedema: lymphatic blockage: breast cancer> lymph nodes removed >
poor drainage
- DVT: Major vessel is occluded and fluid can’t escape

Third Space accumulation

- Fluid in serous cavities: abdominal, peritoneal
- Third spacing – a popular verb for hemorrhage or other accumulation of
fluids into the third space
- Ex: ascites

SIADH – symptoms of inappropriate ADH can lead to edema

Isotonic fluid volume changes

- Isotonic imbalances – fluid volume changes but electrolyte volume conc. are
normal
- Can occur with saline IV or over secretion of aldosterone, excess blood
loss, diaphoresis, fluid loss or reduced fluid intake
- Isotonic dehydration – dry membranes, reduced urine output, hypovolemia,
rapid heard rate, low BP, weight loss, thirst
- Isotonic fluid excess – XS IV fluids, over secretion of aldosterone and
cortisol, hypervolemia, ^ BP,

Hypotonic Hydration
- Excessive waters enters the extracellular space
- Fluid keeps moving and then will enter the cells because it moves to higher
concentration; osmosis
- Is an issue because cells that can’t swell: RBC’s, neurons etc.

Dehydration
- Loss of water > concentration goes up
- Osmotic pressure rises
- Cells lose water and cells shrink due to osmosis
- You will see tenting
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Sodium:
- ADH – kidney
o Particularly in tubules
o Create aquaporins
- Most Na lost through filtrate in kidneys
- Thiazide diuretics > increase Na excretion > drop in plasma volume > drop
in GFR > ^ in water and Na reabsorption in the DCT > compensatory
mechanism
- Need sodium to make bicarb
- Hormone that influences sodium > aldosterone, ANP, BNP -from ventricles

Hyponatremia:
- Serum sodium is less than 135 mEq
- Decrease is caused by decreased concentration

- Hypovolemic Natremia: Low fluid, low sodium

- Deficiency in aldosterone and cortisol
- Lack of aldosterone leads to sodium wasting
- Lack of cortisol increases ADH production
- Can occur in people with adrenal insufficiency
- Aldosterone is released when potassium levels are high. Lack of aldosterone
can lead to metabolic acidosis. WHY?
o Excess K+ outside will move into the cell. The H+ will leave >
metabolic acidosis
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Hypernatremia:
- Above 140 mEq
- Hypertonicity of ECF > cellular dehydration
- Na regulated by kidneys and intestines
- Water loss or increase in Na
- Cerebral cell shrinkage
- Decrease in urine output and urine osmolality is increased
o Retaining water to dilute concentration
- Decreased tissue turgor and thirst
o Hypothalamus signals to drink water to bring concertation back down
to .9
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S&S:

Potassium
- K absorbed in PCT
- Get most from diet > void out a lot
- Insulin, aldosterone, alkalosis, epinephrine > K+ into cell
- Drop in insulin, aldosterone, strenuous exercise, acidosis, cell damage > K
out of cells
o Be able to explain why
- Insulin activates Na-K pump
- Too much aldosterone causes metabolic alkalosis as it causes an increase
in renal excretion of potassium and hydrogen
- Metabolic acidosis leads to hyperkalemia as hydrogen moves into the cells
to be buffered and potassium is released
- As long as there is proper kidney function, you should be able to eliminate
enough K+
- Hyperglycemia causes potassium to shift out of the cells and be lost though
the kidneys due to osmotic diuresis
o High concentrations of glucose and K+ just goes along for the ride

Hypokalemia
- Usually just not getting enough in
- Loss through GI Tract, burns, most common loss is through the kidney
- Redistribution b/t ECF and ICF – insulin increase movement of K and
glucose into cells
- Diuretics
- Mg deficiency; controls gate that prevents K leakage
o K conc. Higher inside and always a chance to leak
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- Aldosterone and cortisol

o Too much > hypokalemia
- Treatment often K+. pills
- Cramps, palpitations
- Rapid infusion of K+ > cardiac arrest
- Alkalosis, arrythmias, tachycardia, irregular rhythm or bradycardia, thread
pulse

Hyperkalemia
- Reduced excretion – renal failure
- Rapid administration
- Decrease in aldosterone; ACE inhibitors > decrease renal excretion of K
o Tendency to retain K+ with ACE inhibitors
- Changes in neuromuscular excitability
- Muscle weakness
- May lead to v-fib and cardiac arrest
- Epinephrine will also tuck K+ out of the cell
Medications: NSAIDS, cellular destruction > K+ is released because it was in the
cells,

Buffers
- Phosphate buffer system inside the cell
- Protein buffer system
o Hemoglobin –
o AA -
o Plasma -
- Bicarb – carbonic acid

- Most ATP is used to make enzymes

Metabolic Acidosis:
- Lactic acidosis – most common form in people in the hospital
o Not oxygenated
o Anaerobic respiration
- Hypoxia > anaerobic respiration with difficulty clearing lactic acid
- Disease related - cancer, diabetes, kidney, heart disease, sepsis, lung
disease, intense exercise
- < 7.35
- 7.2 or less can be fatal
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- Chronic kidney disease most common cause of metabolic acidosis

o Reduces bicarb reabsorption
o Hyperkalemia > reduces NH4 excretion > metabolic acidosis
 Retaining 4 more hydrogen because we cannot get rid of the
ammonia
 Hydrogen cannot leave on its own

Ketoacidosis
- Fat break down > ketoacidosis
- Diabetes
o Diabetic coma but advanced ketoacidosis
o Lack of insulin
- Alcoholic ketoacidosis > oxidation of excess alcohol > acetaldehyde
dehydrogenase in the stomach in liver
o Acetone smell
o Makes breath smell sweet

Alkalosis
- pH above 7.45
- more commonly caused by loss of acid though gastric suctioning or
vomiting
- excessive antacid ingestion
- upper GI bowel obstruction
- diuretics enhance hydrogen secretion
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- renal compensation for metabolic alkalosis, less effective than respiratory

compensation

- shift of hydrogen ions into intracellular space; seen in hypokalemia due to a

low ECF K+ concentration > K+ shifts out of the cell in order to maintain
neutrality > H+ shifts into cells > increase pH > metabolic alkalosis

Respiratory Acidosis
- increase of K+ because it is coming out of the cell into the ECF
- trying to tuck hydrogen away > hyperkalemia
- anything that interferes with breathing rate

Respiratory Alkalosis
- hyperventilation
- excessive aldosterone can lead to alkalosis
o bicarb retention
o hydrogen excretion
o K+ depletion
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