Midterm Review Flashcards
1
Q
Exotoxin vs Endotoxin
A
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
2
Q
Resting membrane potential
Action potential
Depolarization: what shifts, ICF/ECF charge?
Repolarization
Hyperpolization
Refractory period
A
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
3
Q
Difference between osmolarity & osmolality
A
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
4
Q
antidiuretic hormone (ADH)
A
absorbs water in the collecting ducts.
5
Q
Aldosterone
A
released by adrenal cortex
reabsorbs Na, Cl,
Retains water
Excretes K
in renal tubulars
6
Q
Hyponatremia symptoms & causes/diseases
A
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
7
Q
Hypernatremia symptoms and causes
A
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
8
Q
Atrophy:
A
- Atrophy: decreased/shrinkage in cellular size (leg muscle)
9
Q
Hypertrophy:
A
- Hypertrophy: increase in size of cells including the organelles
- Physiological – lift weights
- Pathological – heart muscle, liver, spleen
10
Q
Hyperplasia
A
- Hyperplasia: more cells
- Physiological – menses
- Pathological – beginning of CA, moles
11
Q
Metaplasia
A
- Metaplasia: reversible replacement of mature cell type by another
- Pathological: epithelium in smokers
12
Q
Dysplasia:
A
- Dysplasia: abnormal and irreversible changes in size, shape and organization of mature cells (can lead to CA)
13
Q
Anaplasia
A
Anaplasia: hallmark of cancer cells, poorly differentiate or undifferentiated
14
Q
Directions of ABGs
A
- 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
15
Q
Autosomal Recessive
A
Thalassemia, sickle cell, Wilson’s Disease, hemochromatosis
16
Q
Autosomal Dominant
A
Thalassemia, sickle cell, Wilson’s Disease, hemochromatosis, CF
17
Q
x-link
A
Hemophilia, G6PD (recessive), Robertsonian translocation down syndrome (recessive)
18
Q
Klinefelter Snydrom
A
XXY = 47X
Males with extra X. The Y make them males
male & female sexual chara. - gynecomastia (BC), dec testosterone
Infertility, small testes
Chromosomal Testing
19
Q
Turner Syndrome
A
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
20
Q
Down Syndrome
A
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
21
Q
Glycogen with Burns
A
- Glycogen stores consequence
- Hyperglycemia from glycogen breakdown
- Hypermetabolic state, hyperglycemia
22
Q
types of microcytic anemia
A
iron
thalassemia
Chronic blood loss
Sideroblastic Anemia
23
Q
Iron deficiency
sx and causes
A
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
24
Q
Anisocytosis
Poikylocytosis
A
Anisocytosis (different sizes)
Poikylocytosis (diffent shapes)
25
Thalassemia
**Basophilic stripping.** Poikilocytosis.
Alph: Beta-4 or DNA analysis
Beta: hgb electrophoresis
**No or reduced Globin/small size**
26
types of macrocytic anemia
pernicious/B12
folate
a lack of either alter the synthesis of DNA
27
normocytic types of anemia
anemia of chronic disease
acute blood loss
sicle cell
aplastic
28
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
29
Folate
Glossitis, Spina bifada, NO neurologic
Diet (lack of lentils, green leafy veggies)
MCV very large
30
Sideroblastic Anemia
**No protophoryrin** \> **iron toxicity (bronze skin, cirrhosis)**
Ring Sideroblastin
Myelodysplastic syn., ETOH, INH, lead, zinc; copper def.
31
Aplastic Anemia
pancytopenia
AI \> caused by abnormal T cell inhibition of hematopoisesis
MCV normal
MCH Normal
32
Anemia of chronic disease
RF **(no EPO)**, inflammation, aplastic anemia, hemolytic
33
**_Hemochromatosis_**
1. Primary - Autosomal recessive
2. 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
34
**_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*
35
**_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
36
# test
**Hemophilia**
**types**
**labs for PT, PTT, and BT**
* **Genetic: X-link recessive**, mostly males **X**Y (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
37
**_Thrombocytopenia purpura_**
* **_Thrombocytopenia purpura_**
* Low platelet count = bleeding time (faster) goes up
* Plt count \< 150K
* Immune thrombocytopenia (ITP) : virus
* Thrombotic Thrombocytopenia (TTP): clots
38
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)
39
**_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
40
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
41
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)
42
**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
43
Neutrophils
%
function
Reason for high and low
**_Neutrophilia_ – 50-60%**
**\***_BACTERI_**A**
_\*Initial infection or inflammation_ \> leave puss
\*Increase need – Bands shift to the left (Leukemoid reaction)
_\*macrophage send signal to call neutrophils._ Neutrophils eat**/phagocyte l**ots 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
44
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)**
45
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
1. Cell-Mediated (T-Cells) = Thymus
2. Born (b marrow), mature (thymus), stored (lymph nodes)
46
T-Helper Cells
functions
How they interact with B-cells
1. Functions:
1. Support other Cells
2. **Activate B Cells with** **MHC-II** p. 222
1. **MHC-II: receptor on B-cells**
3. **CD4+ \> HIV attacks CD4+ (no CD4 = no B-cells = no antibodies).**
4. Additionally, hepls neutrophils and macrophages from dying quicker
5. T-cells travel deep inside the lymph node to find B-cells with the correct MHC-II\*\*\*
47
3 sub-types of T-helper
1. _Subtype: **Th1** (Secretes Cytokines)_
1. **Inflammation (TNF)**
2. Cell-mediated Inflammation
3. Virus or Bacteria
2. _Subtype: **Th2** (secretes cytokines)_
1. **Allergy/Parasites**
2. Humoral Immunity/Antibody mediated
3. IL-4, IL-5, IL-13
3. _Subtype: **Th17** (Secretes Cytokines)_
1. Inflammation
2. Wound Healing
3. Fungi
4. IL-17, IL-21, IL-22
48
cytotoxic/killer t-cells/Natural Kill Cells
fx
1. **_Cytotoxic/Killer T-Cells_** Tc (**CD8+** CD3+)
1. Functions
1. Kills cells that have been infiltrated by pathogen (Antigens (Specific) with **MHC-1)**
2. Hitman – machine guns massive killing
3. Don't need previous exposure to identify and kill
49
1. **_Regulatory T-Cells_**
1. **_Regulatory T-Cells_**
1. Police Patroller
2. Maintain tolerance to self-antigens, homeostatis
3. Prevent **_Autoimmune disease_**
50
1. **_Memory T-Cells_**
1. Spy – intelligence monitoring to see if anything is happening
2. Prevent future attacks!
51
B-Cells
growth process
how activated
1. **_B-Cells_** – One function to make antibodies
1. Born (b. marrow), mature (b. marrow), stored (lymph nodes)
2. \*\*\***Activated by T-Helper Cell (with CD4 and MHC-II)**
3. Produce Antibodies (can produce billions of antibodies in 3-4 days)
52
types of antibodies
1. IgA – in tears, breast milk, pass on from mom
2. IgD – no clue
3. IgE – All**e**rgies
4. IgG – Old infections (gold)
5. IgM – Acute Infections (immediate)
53
B-cells two main functions
1. **Two functions of antibodies**
1. **Opsonization:** Attach to pathogens, so they can be recognized and killed. Antibodies “bridge” the gap to phagocytes
2. **Agglutination:** Make pathogens sicky clumpy & neutralizes the location of the antigen
54
Memory B-Cells:
Prevent future attacks/spies
55
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
56
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
57
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
58
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
59
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
60
Compliment system
3 major functions
1. **Compliment system (know general concepts)**
1. Consist of plasma proteins that bind to BACTERIA (primarily) and may start a cascade
2. Removes antigen-antibody complexes
3. Part of the inflammatory response
61
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
62
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
63
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
64
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**
65
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
66
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
67
3 hormones most like to be seen with a pituitary adenoma
all too high
GH \> gigantism/children & acromegaly/adults
Prolactin \> prolactinoma
Cortisol \> Cushings
68
Prolactin
pathway
too much
too little
hypothalamus/prolactin releasing hormone \>
anterior pituitary/prolactin\>
Breast/produces milk
Prolactinoma "pituitary adenoma" - water soluable
prolactin inhibiting hormone
69
cortisol
pathway
too much
too little
hypothalmus/corticotropic releasing hormone \>
ACTH (adrenocorticotropic hormone) \>
adrenal **_cort_**ex \>
**_cort_**isole
(Cushings "pituitary adenoma") or Aldosteronism/Conn dis.
Addision *"need to add cortisole"*
Negative Feedback
70
Hormones released by adrenal cortex
vs
adrenal medulla
Adrenal cortex: (cortisol & aldosterone) - steroids
adrenal medula: catecholamines epinephrine, adrenaline, norepi
71
Aldosterone
lipid solube
released by adrenal cortex
reabsorptio of Na, Cl
excretes K
retaines water
72
Adrenal Medulla
Pheochromocytoms
**_Adrenali_****ne (epi & norepi)** “Med gives epi”
_Actives sympathetic n. system_
**“Pheochromocytoms” \>** Catecholamines \> epi & norepi
**Triad: diaphoresis, episodic HA, tachycarida**
73
posterior pituitary gland
2 hormones
Travel by hypophyseal stalk to posterior pituitary\>\>\>\>\>\>\>\>\>\>\>\>
Anti-diurectic hormone (ADH)
Oxytocin - Wg
74
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
75
Insulin produced by
soluable
beta cells of the pancrease
water soluable
76
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)
77
Melatonin
Produced
fx
produced in the pineal gland
regulates sleep cycles
too much blocks FSH/LH
is stroyed by light
78
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
79
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
80
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*
81
Secondary hyperparathyroidsim
Inc PTH, secondary to **chronic disease**
1) Chronic Reneal Failure
2) dietary deficiency of Vit D & C
**hypercalcemia does not occur**
82
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
83
Pseudohypoparathyroidism
inherited condition \>
normal to elevated PTH
resistent to PTH in the proximal renal tubules
84
Familial hypocalciuric hypercalcemia
Benign autosomal dominant condition
hypercalcemia/hypophos
Low Ca urine
mutation in calcium receptor of the parathyroid gland
85
**_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
86
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**](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
87
RAAS Pathway
88
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**
89
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
90
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)
* **Surgery to remove pituitary gland** & radiation \> may need hormone replacement
91
**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
92
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_
93
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**
94
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
95
**_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
* **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
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**_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
97
Thymus
Hormone produced
funtion
Too little
Thymosin
T-lymphocytes development & production. Also train body to have self-response
too little: AI
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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**
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Secondary hypothyroidism
* deficiency of hypothalamus/thyrotropin-releasing hormone (TRH) and pituitary/TSH
100
**_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
* **_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**
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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
T**X: Thyroid hormone, combined with circulatory and ventilatory support; Management of hyponatremia and hypothermia**
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