Midterm Review Flashcards
Exotoxin vs Endotoxin
Exotoxin: gram pos, proteins released Bacteria Growth
Endotoxin: lipopolysaccharides, gram neg, toxins in the cell wal l> released during lysis > when damage endothelium > hypothalamus/fever, tissue factor III/DIC, & septic shock/vasodialation
- Septic Shock “endotoxin will end in vasodilation, DIC, septic shock”
-
“endo within endothelium” “inside with a fever”
- Gram negative release endotoxins
- Endotoxins: damage endothelium in tissues causing release of PG & leukotrienes from cells. PG & leukotrienes trigger MAST cells to go crazy > Histamine & proteases > vasodilation & incr permeability > lower blood vol. and low BP
- Complement system (C3a & C5a) > vasodilation and permeability.
-
WBC come to fight > Phagocytes release
- IL-1 & TNF-alpha > hypothalamus > PGE2 > Fever
- IL-6 > liver > acute phase reactant proteins (makes liver more responsive to filter endotoxins out)
- IL-8 > backups > more phagocytosis
- Microvascular occlusion > ischemia
- Increase tissue factor (factor III) > DIC
- s/s: low BP, low SVR, HIGH CO (tachy, heart working properly), High O2 sat (low O2 delivery, hypoxia)
- Ceftriaxone/Zosyn, Bcx, isotonic fluids (NS or LR), vasopressors
- Gram negative release endotoxins
Resting membrane potential
Action potential
Depolarization: what shifts, ICF/ECF charge?
Repolarization
Hyperpolization
Refractory period
All body cells are more negatively charged than ECF (electrical polarizity)
Resting membrane potential: the difference in electrical changes inside (ICF) and outside of the cell (ECF) -70. More permeable to potassum
N. and M. cells can change resting potential
Action potential: opening voltage gates/sodium gates, occurs during depolization; changes cell from negative to positive.
Depolarization: cell now more positively charged then ECF; Na+ enters cell
Repolarization: K leaves the cell and returns to resting membrane potential
Hyperpolization: toom much K leaves the cell
Absolute Refractory period: another action potential can’t happen
Difference between osmolarity & osmolality
Osmolarity: number of solutes/liter (milliosomoles per liter; mOsm or molecules per liter)
Osmolality: weight of solute in liquid (won’t change); better oncotic measurement
antidiuretic hormone (ADH)
absorbs water in the collecting ducts.
Aldosterone
released by adrenal cortex
reabsorbs Na, Cl,
Retains water
Excretes K
in renal tubulars
Hyponatremia symptoms & causes/diseases
s/s: peripheral/cerebral edema (wt gain), HA, lethargy, restlessness, m. weakness, ALOC, Sz, Cells Swell (osmosis causes water to leave ECF and go into intracellular fluid)
Causes: diuretics, V/D/Sweating, Addison’s disease (primary adrenal insuff.), hypopituitary (2nd adrenal insuff.), SIADH, CHF, kidney pathologies
Addision’s insufficent cortisol
Hypernatremia symptoms and causes
low grade fever, flushed skin; restless/irritable; increased fluid retention and BP; peripheral and pitting edema; decreased urine output, dry mouth
Causes: corticosteroids, Cushing’s disease, hyperaldosteronism, dehydration, DI (types)
Cells shrink
Atrophy:
- Atrophy: decreased/shrinkage in cellular size (leg muscle)
Hypertrophy:
- Hypertrophy: increase in size of cells including the organelles
- Physiological – lift weights
- Pathological – heart muscle, liver, spleen
Hyperplasia
- Hyperplasia: more cells
- Physiological – menses
- Pathological – beginning of CA, moles
Metaplasia
- Metaplasia: reversible replacement of mature cell type by another
- Pathological: epithelium in smokers
Dysplasia:
- Dysplasia: abnormal and irreversible changes in size, shape and organization of mature cells (can lead to CA)
Anaplasia
Anaplasia: hallmark of cancer cells, poorly differentiate or undifferentiated
Directions of ABGs
- Anion Gap: Na-(Cl+HCO)= 10-12
- *10-12: Cl- increase to compensate = Renal/GI loss of HCO or dec H+
- *>12: MUDPILES
- Metabolic: pH, pCO2 same direction
- Resp pH, pCO2 opposite direction
Autosomal Recessive
Thalassemia, sickle cell, Wilson’s Disease, hemochromatosis
Autosomal Dominant
Thalassemia, sickle cell, Wilson’s Disease, hemochromatosis, CF
x-link
Hemophilia, G6PD (recessive), Robertsonian translocation down syndrome (recessive)
Klinefelter Snydrom
XXY = 47X
Males with extra X. The Y make them males
male & female sexual chara. - gynecomastia (BC), dec testosterone
Infertility, small testes
Chromosomal Testing
Turner Syndrome
45X = X_
short, no/irreg menstrual
no breast development, wide spaced nipples
infertility
Webbed Neck, low posterior hair line
Infants swollen hands and feet
Tx: GH & estrogen
Down Syndrome
XXX, Trisomy 21
95% non-disjunction (chromosomes don’t pull apart in metaphase)
1% mosaic
4% Translocation
Single cease in palms (Simian crease)
Heart defects, ALL
25% over 35yo dementia
may have decrease IQ & speech difficulties
Testing: amniocentesis, karyotype test
Glycogen with Burns
- Glycogen stores consequence
- Hyperglycemia from glycogen breakdown
- Hypermetabolic state, hyperglycemia
types of microcytic anemia
iron
thalassemia
Chronic blood loss
Sideroblastic Anemia
Iron deficiency
sx and causes
sx: Kaoilonychia (bumpy nail), alopecia, tongue (shiny, red, no papillae), angular stomatitis, Inc HR, fatitue, pallor, or asymptomatic
low iron: diet, celiac, chronic diarrhea, low gastric HCL; increase requirements (infants, children/adolescents, menses, pregr). Chronic blood loss
MCV <80
MCH <27
TIBC High
Anisocytosis
Poikylocytosis
Anisocytosis (different sizes)
Poikylocytosis (diffent shapes)
Thalassemia
Basophilic stripping. Poikilocytosis.
Alph: Beta-4 or DNA analysis
Beta: hgb electrophoresis
No or reduced Globin/small size
types of macrocytic anemia
pernicious/B12
folate
a lack of either alter the synthesis of DNA
normocytic types of anemia
anemia of chronic disease
acute blood loss
sicle cell
aplastic
Pernicious/B12
Schilling test: ID pernicious anemia
demyelination (paresthesia of fingers & toes)
IF deficiency (congenital, atrophic gastritis, AI); celiac, IBD; Metformin
MCV > 100 very large
MCH normal
Fe normal
Folate
Glossitis, Spina bifada, NO neurologic
Diet (lack of lentils, green leafy veggies)
MCV very large
Sideroblastic Anemia
No protophoryrin > iron toxicity (bronze skin, cirrhosis)
Ring Sideroblastin
Myelodysplastic syn., ETOH, INH, lead, zinc; copper def.
Aplastic Anemia
pancytopenia
AI > caused by abnormal T cell inhibition of hematopoisesis
MCV normal
MCH Normal
Anemia of chronic disease
RF (no EPO), inflammation, aplastic anemia, hemolytic
Hemochromatosis
- Primary - Autosomal recessive
- Secondary – etoh, blood transfusion
- Sx: fatigue, arthritis, gray or bronze skin tone
- Iron deposits in liver, pancreas, heart, joints/arthritis, anterior pituitary
- Labs: high iron, ferritin, transferrin saturation, and TIBC
Hemosiderosis:
- Overload of iron in organs & tissues (different from hemochromatosis)
- Results from
- bleeding into tissues > breakdown of RBCs
- destruction of RBCs in blood vessels
- Hemolytic anemia
- Hemochromatosis
- Fatty liver disease
- Transfusions
Aplastic Anemia
Normalcytic, normalchromic
*pancytopenia with empty marrow
*Most idiopathic – autoimmune disease > abnormal T cell inhibition of hematopoisesis
*Treatment:
1) IS (CSA and antithymocyte globulin)
2) allogenic BMT
Irradiate CMV negative blood products until CMV status known
test
Hemophilia
types
labs for PT, PTT, and BT
- Genetic: X-link recessive, mostly males XY (get from mom); both parents must have disease to get as a female
- still have platelets, just no fibrin
- Type A (classic hemophilia): 80%, lack factor VIII (don’t have part of positive feedback) A8
- Type B (Christmas Disease): 15%, lack factor IX (have all of positive feedback, so less serious) B9 “be Marry”
- Bleed long, not faster
- Infants bruising with mild irritation.
- Umbilical cord bleeds excessively
- Older noses bleeds easy bruising, blood in urine, severe joint pain, joint surgery
- Labs: Inc PTT, normal PT and bleeding time (normal bleeding time = how fast you bleed out) > bleed out longer
- Testing: Inc PTT, normal PT/BT, Factor 8 or 9
Thrombocytopenia purpura
- Thrombocytopenia purpura
- Low platelet count = bleeding time (faster) goes up
- Plt count < 150K
- Immune thrombocytopenia (ITP) : virus
- Thrombotic Thrombocytopenia (TTP): clots
Polycythemia Vera
- Too many RBCs
- Abnormal, idiopathic
- S/S hyperviscosity, splenomegaly, thrombi, infarct, HA, Pruritis after warm bath/shower, plethora (ruddy complexion) in the face, palms, nailbeds, mucosa, and conjunctive. tinnitus, chorea, delirium, visual disturbance, angina, thrombosis, ischemia
- Test: CBC
- Tx: phlebotomy (blood letting)
Von Willebrand’s Disease
- Genetic: autosomal dominant
- Don’t have Von Willebrand factor
- Platelets don’t clump together
- vWF is needed to make platelet aggregate and adhere (inadequate platelet plug = prolong bleeding)
- Labs: Incr PTT and bleeding time, but PT and PLT normal
- Positive vWF antigen
Discuss disseminated intravascular disorder (DIC).
- Lots of tissue factor III (Extrinsic pathway) released, which is not normally in blood
- D-dimer goes up
- Widespread clotting > consumes platelets & clotting factors leading to hemorrhage
- Clotting and bleeding at the same time
- Causes: sepsis, bacterial infections, cancer, placenta retained or abruptions, anesthesia, burns, major trauma
- Inc PT, Inc PTT, inc lactic dehydrogenase, inc creatinine
- Dec PLT, dec fibrinogen, protein C or S, pH, PaO2
- Inc D-dimer (break down products of fibrin)
- Subacute hemorrhage and diffuse microcirculatory thrombosis
- Sepsis most common cause, trauma, CASIR, placental abruptions, preeclampsia
- Release tissue factor by the endothelium
RBC life Cycle
- Kidney detects hypoxia> sends erythropoietin (EPO) > b. marrow in long bone produce reticulocytes (24-48hr) > RBCs (kids 60days, toddler 90 days, adults 120) > spleen > recycle globin and send heme to liver > heme turns into bilirubin > intestines
- EPO to RBC = 1 week
- *important in evaluating for possible pathologies (high CA?, low production issue)
Clotthing pathway
PTT
PT
Postive Feedback
Negative feedback
Platelet and Clotting Disorders
- Injury to bl vessels > vasodilation to bring bl to the area > platelets stick together with collagen (platelet plug) > Fibrin (a string of protein) needs factor XIII(A)
- aPTT = Intrinsic pathway (in a relationship), heparin
- PT = Extrinsic pathway (out of a relationship), warfarin
Neutrophils
%
function
Reason for high and low
Neutrophilia – 50-60%
*BACTERIA
*Initial infection or inflammation > leave puss
*Increase need – Bands shift to the left (Leukemoid reaction)
*macrophage send signal to call neutrophils. Neutrophils eat/phagocyte lots bacteria and die (suicide bomber). Often *Macrophages and neutrophils can fight most infections.
*T-Helper cells support neutrophils and macrophages from dying quicker
Neutropenia
*Primary: congenital or acquired (leukemia)
*Secondary: IS disorders or IS meds
Lymphocytes %
function
High and low reasons
(types in different cards)
Lymphocytosis (T & B-Cells) 30%
*Acute VIRAL infections (ex. Epstein-Barr virus)
*Leukemia, lymphomas, some chronic infections
Lymphocytopenia
*immune deficiencies, drug destructions, viral destruction
*radiation or acquired immunodeficiency disorders (AIDS)
4 types of T-Cell
where they grow and live
fx in other flashcards
T-Helper
Cytotoxic/Killer T-cell
Memory T-cells
Regulatory T-Cells
- Cell-Mediated (T-Cells) = Thymus
- Born (b marrow), mature (thymus), stored (lymph nodes)
T-Helper Cells
functions
How they interact with B-cells
- Functions:
- Support other Cells
-
Activate B Cells with MHC-II p. 222
- MHC-II: receptor on B-cells
- CD4+ > HIV attacks CD4+ (no CD4 = no B-cells = no antibodies).
- Additionally, hepls neutrophils and macrophages from dying quicker
- T-cells travel deep inside the lymph node to find B-cells with the correct MHC-II***
3 sub-types of T-helper
-
Subtype: Th1 (Secretes Cytokines)
- Inflammation (TNF)
- Cell-mediated Inflammation
- Virus or Bacteria
-
Subtype: Th2 (secretes cytokines)
- Allergy/Parasites
- Humoral Immunity/Antibody mediated
- IL-4, IL-5, IL-13
-
Subtype: Th17 (Secretes Cytokines)
- Inflammation
- Wound Healing
- Fungi
- IL-17, IL-21, IL-22
cytotoxic/killer t-cells/Natural Kill Cells
fx
-
Cytotoxic/Killer T-Cells Tc (CD8+ CD3+)
- Functions
- Kills cells that have been infiltrated by pathogen (Antigens (Specific) with MHC-1)
- Hitman – machine guns massive killing
- Don’t need previous exposure to identify and kill
- Functions
- Regulatory T-Cells
-
Regulatory T-Cells
- Police Patroller
- Maintain tolerance to self-antigens, homeostatis
- Prevent Autoimmune disease
- Memory T-Cells
- Spy – intelligence monitoring to see if anything is happening
- Prevent future attacks!
B-Cells
growth process
how activated
-
B-Cells – One function to make antibodies
- Born (b. marrow), mature (b. marrow), stored (lymph nodes)
- ***Activated by T-Helper Cell (with CD4 and MHC-II)
- Produce Antibodies (can produce billions of antibodies in 3-4 days)
types of antibodies
- IgA – in tears, breast milk, pass on from mom
- IgD – no clue
- IgE – Allergies
- IgG – Old infections (gold)
- IgM – Acute Infections (immediate)
B-cells two main functions
-
Two functions of antibodies
- Opsonization: Attach to pathogens, so they can be recognized and killed. Antibodies “bridge” the gap to phagocytes
- Agglutination: Make pathogens sicky clumpy & neutralizes the location of the antigen
Memory B-Cells:
Prevent future attacks/spies
monocytes
%
fx
high and low
Monocytosis 3-7%
*Usually occurs with neutropenia in the later stages of a bacterial infection
*chronic infections and correlates with extent of myocardial damage
*Monocytes turn into macrophages and dendritic cells
Monocytopenia
*Very little known about this condition
*Prednisone treatment
Eosinophils
Eosinophilia 2%(memorize all 3)
*Hypersensitivity reaction
*allergic reaction
*Parasites (may not so in eosinophiles)
Eosinopenia
*primary cause – migration of cells to inflammatory sites
Basophils
Basophilia 0-1%
*Inflammation and hypersensitivity reactions > HISTAMINE
(Histamine also produced by mast cells)
Basopenia
*Acute infections, hyperthyroidism, and long-term steroid therapy
*Hairy cell Leukemia
Macrophages
immune system type
fx
single
produce
- Macrophages: innate immune system. (first responders and can often resolve infection on their own) eat pathogens (phagocytosis), looks like Packman. Macrophages will eat everything not the host (good and bad bacteria). Live in tissues. If they cannot fight off infections, Macrophages single PG, NO
- Produce TNF
Fx of PG, NO
-
Vasodilation caused by PG and NO
- Release water/edema
- Slow down bacteria &
- Helps transport response immune cells to enter tissue)
- Complement to Tc
Compliment system
3 major functions
-
Compliment system (know general concepts)
- Consist of plasma proteins that bind to BACTERIA (primarily) and may start a cascade
- Removes antigen-antibody complexes
- Part of the inflammatory response
RBC count
thrombocyte count
leukocytes order high to low
Which ones are grandulocytes
Erythrocytes 4-6 mil/mm3
Thrombocytes 140,000-340,000/mm3 (live 10 days)
Leukocytes 5,000 – 10,000/mm3
Neutrophils 60%
Lymphocytes 30%
Monocytes 5%
Esosinophils 2%
Basophils 0-1%
“Never Let Monkey Eat Banana “ said Grandpa Ben
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
Hypersensitivity Reactions
Type I: IgE - Allergic - meds, bees, latex
Type II: cytotoic - antibody-mediate - hemolytic reactions
Type III: IgG, IgM - Immune complex depositions - lupus
Type IV: Delayed, cell-mediated - graft rejections
Thyroid pathway
too much
too little
Hypothalamus/thyrotropin releasing hormone >
Anterior Pituitary/Thyroid stimulating hormone >
Thyroid Glad/T3 & T4 >
Hyperthyroidism, Grave’s, Thyrotix crisis
Hashimoto, subacute throiditis/virus, iodine deficiency
Negative Feedback
sex hormones
too much
too little
Hypothalamus/gonadotropin releasing hormone >
anterior pituitary/Follic stimulating hormone, & luteinizing hormone
Estrogen-L & testosterone-L
Cancer (ex Breast CA)
PCOS
lack of sec chara.
POSTIVE FEEDBACK
Calcintonin
where it is screted
what it does
secreted by thyroid gland
decreases blood calcium by:
stimulates osteoclasts to deposit Ca in b. & reduce absorption by kidneys
“building calcium in bones”
Water soluable
Growth Hormone
Pathway
too much
too little
hypothalamus/growth hormone releasing hormone >
anterior pituitary/growth hormone (water) >
goes to entire body
gigantism/children & acromegaly/adults > pituitary adenoma
dwarfism
Somatostatin inhibits GH & TSH
3 hormones most like to be seen with a pituitary adenoma
all too high
GH > gigantism/children & acromegaly/adults
Prolactin > prolactinoma
Cortisol > Cushings
Prolactin
pathway
too much
too little
hypothalamus/prolactin releasing hormone >
anterior pituitary/prolactin>
Breast/produces milk
Prolactinoma “pituitary adenoma” - water soluable
prolactin inhibiting hormone
cortisol
pathway
too much
too little
hypothalmus/corticotropic releasing hormone >
ACTH (adrenocorticotropic hormone) >
adrenal cortex >
cortisole
(Cushings “pituitary adenoma”) or Aldosteronism/Conn dis.
Addision “need to add cortisole”
Negative Feedback
Hormones released by adrenal cortex
vs
adrenal medulla
Adrenal cortex: (cortisol & aldosterone) - steroids
adrenal medula: catecholamines epinephrine, adrenaline, norepi
Aldosterone
lipid solube
released by adrenal cortex
reabsorptio of Na, Cl
excretes K
retaines water
Adrenal Medulla
Pheochromocytoms
Adrenaline (epi & norepi) “Med gives epi”
Actives sympathetic n. system
“Pheochromocytoms” > Catecholamines > epi & norepi
Triad: diaphoresis, episodic HA, tachycarida
posterior pituitary gland
2 hormones
Travel by hypophyseal stalk to posterior pituitary>>>>>>>>>>>>
Anti-diurectic hormone (ADH)
Oxytocin - Wg
ADH Pathway
function
released by
too much
too little
Produced in hypothalamus >
Stored & released in POSTERIOR pituitary
ADH/vasopressin: works in kidneys to reabsorb water > Inc BP
SIADH
DI
Insulin produced by
soluable
beta cells of the pancrease
water soluable
Glucagon
Produced
Produced in alpha cells of pancrease & by GI lining
Increase BG by gluconeogensis in liver
Glycogen stored in liver
Antagonist to insulin > causes cells to release glucose from glycogen (gluconeogenesis in live & stim lipolysis)
Melatonin
Produced
fx
produced in the pineal gland
regulates sleep cycles
too much blocks FSH/LH
is stroyed by light
Parathyroid
pathway
too high
too low
low blood calcium levels >
PTH > Inc Ca from b. (osteoclasts), tubules of nephrons, & intestines
too much PTH > hypercalcemia/hypophos
too high: hypercalcemia
too low > hypoparathyroidism = hypocalcemia/hypophos
Chvostek and Trousseau signs
Chvostek (Cheek): elicited by tapping the cheek, resulting in twitching of the upper lip.
Trousseau signs (Tourniquet/BP): elected by sustained inflation of a sphygmomanoeter placed on the upper arm to a level above systolic BP with resultant painful carpal spasm
exam question
Primary Hyperparathyroidism
Primary hyperparathyroidsm: too mch PTH from parathyroid gland. 80-85% parathyroid adenomas - one of the most commone endocrine disorders
- *reabsorption of Ca from b.*
- * increase absorption from intestines*
- Hallmarks: hypercalcemia, hypophos*
Secondary hyperparathyroidsim
Inc PTH, secondary to chronic disease
1) Chronic Reneal Failure
2) dietary deficiency of Vit D & C
hypercalcemia does not occur
Tertiary hyperparatheyroidism
develops after any long-standing period of hypoocalcemia (HD, GI malabsoprtion). from long-standing secondary hyperparathyroidism
prolonged hypocalcemia casues hyperplasia in parathyroid chief cell > excessive PTH
commonly seen after renal transplant
will have normal or hypercalcemia
Pseudohypoparathyroidism
inherited condition >
normal to elevated PTH
resistent to PTH in the proximal renal tubules
Familial hypocalciuric hypercalcemia
Benign autosomal dominant condition
hypercalcemia/hypophos
Low Ca urine
mutation in calcium receptor of the parathyroid gland
Hyperparathyroidism – s/s & treatment
- Most asymptomatic
- Hypercalcemia and hypophosphatemia, possible kidney stones from hypercalciuria, alkaline urine, pathologic fractures
- Secondary: Low serum calcium but elevated PTH
- Treatment: Surgery, bisphosphonates, corticosteroids, and calcimimetics
hypoparathyroidsim
- low PTH levels
- Usual causes: Parathyroid damage in thyroid surgery, autoimmunity, or genetic mechanisms
- Clinical manifestations
- dec serum calcium & Inc phosphate level
- Lowering of the threshold for nerve and muscle excitation Muscle spasms; hyperreflexia; tonic-clonic convulsions; laryngeal spasms; death from asphyxiation
- Chvostek (Cheek) and Trousseau signs (Tourniquet/BP): exam question https://www.youtube.com/watch?v=iTPPP89A1TA
- Chvostek (Cheek): elicited by tapping the cheek, resulting in twitching of the upper lip.
- Trousseau signs (Tourniquet/BP): elected by sustained inflation of a sphygmomanoeter placed on the upper arm to a level above systolic BP with resultant painful carpal spasm
- Tx: Calcium, vitamin D, and poss Phosphate binders
RAAS Pathway
SIADH
- SIADH: Oliguria, HTN
- Na < 135 mEq/L (110 – 115 severe, possibly irreversible, neurologic damage)
- Urine osmolarity Incr (concentrated urine), = greater than serum osmolarity
- Serum/blood osmolarity Dec < 280 mOsm/kg
- 3P: Most common cause of SIADH is lung or abdominal cancer > releases hormone similar to ADH. Also sometimes after surgery.
- Posterior Pituitary > Action of ADH on renal collecting ducts increases their permeability to water, thus increasing water reabsorption
- Other cause: after surgery
- Treat: hypertonic saline, conivaptan, fluid restriction 800 – 1000/day, chronic SIADH demeclocycline
DI
- DI: polyuria, hypotension
- Characterized by the inability of the kidney to increase permeability to water
- Polyuria, Polydipsia, nocturia, continual thirst
- Na>135
- 12-15 liters (Normal 1-2 liters) of urine a day
- Diabetes referring to urine
- Urine osmolarity down (diluted)
- Urine specific gravity <1.010
- Urine osmolality <200 mOsml/kg
- Inc Plasma osmolality > 300 mOsm or more
- Causes:
- neurogenic (insufficient ADH) > DDAVP (synthetic vasopressin),
- inability to concentrate urine > tx reversible disorders (meds, electrolytes), thiazide
- nephrogenic (insensitivity of the renal collecting tubules to ADH),
- dipsogenic (excessive fluid intaking, lowing plasma osmolarity to the point that it falls below the threshold for ADH secretion) > effective mgt of water ingestion
Hyperpituitarism
s/s
3 most common hormones & syndromes
Treatment
- HA & fatigue, visual changes
- Commonly from benign, slow-growing pituitary adenoma
- Pituitary Adenoma
- S/S: N/V, HA & fatigue, visual changes (tumor pressing on optic nerve crossing)
-
3 most common Incr Hormones:
-
Prolactin: 30%, galactorrhea
- Most common hormonally active pituitary tumor
- Hypogonadsims
- Cabergoline
- ACTH: Cushings syndrome
-
GH:
- Gigantism in children & adolescents (epiphyseal plates open)
- Acromegaly in Adults (epiphyseal plates have closed) > enlarged facial bones, hands, and feet. Protrusion of the lower jaw and forehead. Need new shoes, hats, rings, or gloves
- GH also helps muscles grow > cardiac hypertrophy; hypertension; atherosclerosis; DMII > coronary artery disease
- Octreotide (somatostatin) to lower GH levels
- Pegvisomant (blocks GH receptor)
-
Prolactin: 30%, galactorrhea
- Surgery to remove pituitary gland & radiation > may need hormone replacement
Primary Hypofunction of the Adrenal Cortex
-
Addison disease - adrenal cortex not working, plenty of ACTH (adrenocorticotropic hormone)
- Primary – adrenal insufficiency – hypercortisolism
- Rare, AI
- S/s:
- Elevated ACTH (adrenal cortex not working)
- Hypocortisolism, hyoaldosteronism, weakness, hyperpigmentation (skin, nails & gums), vitiligo
- Test: ACTH stimulation test. Let pt convert cortisol by themselves. (Never give cortisol > kill pt)
- Tx: lifte time glucocorticoid & mineralocorticoid daily replacement
Secondary Hypofunction of the Adrenal Cortex
-
Secondary hypercortisolism
- prolonged administration of exogenous glucocorticoids, which suppress ACTH secretion. S/s similar to Addision, except NO hyperpigmentation
Thyrotoxicosis
Hyperthyroidism: Thyrotoxicosis
- Increased metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by the sympathetic nervous system; enlargement of the thyroid gland (goiter)
- Tx: methimazole or propylthiouracil (antithyroid drug), Radioactive iodine therapy, Surgery
Graves
Hyperthyroidism: Graves disease
- AI, develops autoantibodies
- s/s: exophthalmos (orbital fat accumulation), Diplopia (double vision), Pretibial myxedema (Leg swelling, graves dermopathy).
- Tx: antithyroid drugs, radioactive iodine, or surgery > expothalmos & pretibial myxedema are not reversed
Hyperthyroidism – nodular thyroid disease
- Two types
-
Toxic multinodular goiter (TNG): multiple hyperfunctioning nodules that secrete thyroid h.
- Hot nodules: uptakes radioactive iodine -?
- Cold nodules: not causing issues
- Solitary toxic adenoma: one nodule becomes hyperfunctioning
-
Toxic multinodular goiter (TNG): multiple hyperfunctioning nodules that secrete thyroid h.
- symptoms occur slowly and are the same as hyperthyroidism
- Note the difference b/n Graves & nodular thyroid disease
Tx: antithyroid drugs, radioactive iodine, or surgery
Thyrotoxic crisis (thyroid storm) – test question
- Life threatening within 48 hours
- Results from excessive stress, infection, surgery (esp thyroid), OB complication, HD – too much T4 & T3
- s/s: tachycardia, especially atrial tachydysrhythmias; high-output heart failure; agitation/delirium; N/V, diarrhea> dehydration
- Tx: methimazole or propylthiouracil (antithyroid drug), beta-blocker, corticosteroids, potassium iodide; PTU inhibits the enzyme thyroperoxidase, which normally acts in thyroid hormone synthesis; Saturated solution of KI à In hyperthyroid patients, iodine acutely inhibits hormonal secretion within hours, but the responsible mechanisms are uncertain
Thymus
Hormone produced
funtion
Too little
Thymosin
T-lymphocytes development & production. Also train body to have self-response
too little: AI
4 hypothroidsim primary reasons
Hypothyroidism - Primary
- Iodine deficiency (endemic goiter): Most common worldwide
- Autoimmune thyroiditis (Hashimoto disease): Most common hypothyroidism in the United States
-
Congenital hypothyroidism
- If not treated, cretinism develops > Neonatal screening to reduce incidents
- Administration of T4
-
Thyroid carcinoma
- Most common endocrine malignancy from ionizing radiation
- Changes in voice and swallowing and difficulty in breathing, related to a tumor growth impinging the trachea or esophagus
- Some may have normal T3 and T4 levels
-
Subacute De Quervain’s Thyroiditis:
- Caused: virus, URI > inflammation of thyroid
- S/S: neck pain, virus sxs, Transient hyperthyroidism followed by transient asymptomatic hypothyroidism_, No_ myxedema, Complete recovery
- Testing: Thyroid Ab negative
Secondary hypothyroidism
- deficiency of hypothalamus/thyrotropin-releasing hormone (TRH) and pituitary/TSH
Hypothyroidism - s/s & Treatment
- Levothyroxine
- low metabolism, cold intolerance, fatigue, slightly lower basal body temperature
- Myxedema: nonpitting, boggy edema, especially around the eyes, hands, and feet; thickening of the tongue
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Myxedema coma: Medical Emergency > DLOC, hypothermia w/o shivering, hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma
- TX: Thyroid hormone, combined with circulatory and ventilatory support; Management of hyponatremia and hypothermia
Myxedema & Myxedema Coma
Myxedema: nonpitting, boggy edema, especially around the eyes, hands, and feet; thickening of the tongue
Myxedema coma: Medical Emergency > DLOC, hypothermia w/o shivering, hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma
TX: Thyroid hormone, combined with circulatory and ventilatory support; Management of hyponatremia and hypothermia
