Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Midterm Review > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

antidiuretic hormone (ADH)

A

absorbs water in the collecting ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aldosterone

A

released by adrenal cortex

reabsorbs Na, Cl,

Retains water

Excretes K

in renal tubulars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Atrophy:

A
  • Atrophy: decreased/shrinkage in cellular size (leg muscle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypertrophy:

A
  • Hypertrophy: increase in size of cells including the organelles
    • Physiological – lift weights
    • Pathological – heart muscle, liver, spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hyperplasia

A
  • Hyperplasia: more cells
    • Physiological – menses
    • Pathological – beginning of CA, moles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Metaplasia

A
  • Metaplasia: reversible replacement of mature cell type by another
    • Pathological: epithelium in smokers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dysplasia:

A
  • Dysplasia: abnormal and irreversible changes in size, shape and organization of mature cells (can lead to CA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anaplasia

A

Anaplasia: hallmark of cancer cells, poorly differentiate or undifferentiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Autosomal Recessive

A

Thalassemia, sickle cell, Wilson’s Disease, hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Autosomal Dominant

A

Thalassemia, sickle cell, Wilson’s Disease, hemochromatosis, CF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

x-link

A

Hemophilia, G6PD (recessive), Robertsonian translocation down syndrome (recessive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Glycogen with Burns

A
  • Glycogen stores consequence
    • Hyperglycemia from glycogen breakdown
    • Hypermetabolic state, hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

types of microcytic anemia

A

iron

thalassemia

Chronic blood loss

Sideroblastic Anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Anisocytosis

Poikylocytosis

A

Anisocytosis (different sizes)

Poikylocytosis (diffent shapes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Thalassemia

A

Basophilic stripping. Poikilocytosis.

Alph: Beta-4 or DNA analysis

Beta: hgb electrophoresis

No or reduced Globin/small size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

types of macrocytic anemia

A

pernicious/B12

folate

a lack of either alter the synthesis of DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

normocytic types of anemia

A

anemia of chronic disease

acute blood loss

sicle cell

aplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pernicious/B12

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Folate

A

Glossitis, Spina bifada, NO neurologic

Diet (lack of lentils, green leafy veggies)

MCV very large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Sideroblastic Anemia

A

No protophoryrin > iron toxicity (bronze skin, cirrhosis)

Ring Sideroblastin

Myelodysplastic syn., ETOH, INH, lead, zinc; copper def.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Aplastic Anemia

A

pancytopenia

AI > caused by abnormal T cell inhibition of hematopoisesis

MCV normal

MCH Normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Anemia of chronic disease

A

RF (no EPO), inflammation, aplastic anemia, hemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hemochromatosis

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Hemosiderosis:

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Aplastic Anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

test

Hemophilia

types

labs for PT, PTT, and BT

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Thrombocytopenia purpura

A
  • Thrombocytopenia purpura
  • Low platelet count = bleeding time (faster) goes up
  • Plt count < 150K
  • Immune thrombocytopenia (ITP) : virus
  • Thrombotic Thrombocytopenia (TTP): clots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Polycythemia Vera

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Von Willebrand’s Disease

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Discuss disseminated intravascular disorder (DIC).

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

RBC life Cycle

A
  • 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
Q

Clotthing pathway

PTT

PT

Postive Feedback

Negative feedback

A

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
Q

Neutrophils

%

function

Reason for high and low

A

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

44
Q

Lymphocytes %

function

High and low reasons

(types in different cards)

A

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
Q

4 types of T-Cell

where they grow and live

fx in other flashcards

A

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
Q

T-Helper Cells

functions

How they interact with B-cells

A
  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
Q

3 sub-types of T-helper

A
  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
Q

cytotoxic/killer t-cells/Natural Kill Cells

fx

A
  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
Q
  1. Regulatory T-Cells
A
  1. Regulatory T-Cells
    1. Police Patroller
    2. Maintain tolerance to self-antigens, homeostatis
    3. Prevent Autoimmune disease
50
Q
  1. Memory T-Cells
A
  1. Spy – intelligence monitoring to see if anything is happening
  2. Prevent future attacks!
51
Q

B-Cells

growth process

how activated

A
  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
Q

types of antibodies

A
  1. IgA – in tears, breast milk, pass on from mom
  2. IgD – no clue
  3. IgE – Allergies
  4. IgG – Old infections (gold)
  5. IgM – Acute Infections (immediate)
53
Q

B-cells two main functions

A
  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
Q

Memory B-Cells:

A

Prevent future attacks/spies

55
Q

monocytes

%

fx

high and low

A

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
Q

Eosinophils

A

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
Q

Basophils

A

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
Q

Macrophages

immune system type

fx

single

produce

A
  • 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
Q

Fx of PG, NO

A
  • Vasodilation caused by PG and NO
    • Release water/edema
    • Slow down bacteria &
    • Helps transport response immune cells to enter tissue)
    • Complement to Tc
60
Q

Compliment system

3 major functions

A
  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
Q

RBC count

thrombocyte count

leukocytes order high to low

Which ones are grandulocytes

A

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
Q

Hypersensitivity Reactions

A

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
Q

Thyroid pathway

too much

too little

A

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
Q

sex hormones

too much

too little

A

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
Q

Calcintonin

where it is screted

what it does

A

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
Q

Growth Hormone

Pathway

too much

too little

A

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
Q

3 hormones most like to be seen with a pituitary adenoma

A

all too high

GH > gigantism/children & acromegaly/adults

Prolactin > prolactinoma

Cortisol > Cushings

68
Q

Prolactin

pathway

too much

too little

A

hypothalamus/prolactin releasing hormone >

anterior pituitary/prolactin>

Breast/produces milk

Prolactinoma “pituitary adenoma” - water soluable

prolactin inhibiting hormone

69
Q

cortisol

pathway

too much

too little

A

hypothalmus/corticotropic releasing hormone >

ACTH (adrenocorticotropic hormone) >

adrenal cortex >

cortisole

(Cushings “pituitary adenoma”) or Aldosteronism/Conn dis.

Addision “need to add cortisole”

Negative Feedback

70
Q

Hormones released by adrenal cortex

vs

adrenal medulla

A

Adrenal cortex: (cortisol & aldosterone) - steroids

adrenal medula: catecholamines epinephrine, adrenaline, norepi

71
Q

Aldosterone

A

lipid solube

released by adrenal cortex

reabsorptio of Na, Cl

excretes K

retaines water

72
Q

Adrenal Medulla

Pheochromocytoms

A

Adrenaline (epi & norepi) “Med gives epi”

Actives sympathetic n. system

“Pheochromocytoms” > Catecholamines > epi & norepi

Triad: diaphoresis, episodic HA, tachycarida

73
Q

posterior pituitary gland

2 hormones

A

Travel by hypophyseal stalk to posterior pituitary>>>>>>>>>>>>

Anti-diurectic hormone (ADH)

Oxytocin - Wg

74
Q

ADH Pathway

function

released by

too much

too little

A

Produced in hypothalamus >

Stored & released in POSTERIOR pituitary

ADH/vasopressin: works in kidneys to reabsorb water > Inc BP

SIADH

DI

75
Q

Insulin produced by

soluable

A

beta cells of the pancrease

water soluable

76
Q

Glucagon

Produced

A

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
Q

Melatonin

Produced

fx

A

produced in the pineal gland

regulates sleep cycles

too much blocks FSH/LH

is stroyed by light

78
Q

Parathyroid

pathway

too high

too low

A

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
Q

Chvostek and Trousseau signs

A

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
Q

Primary Hyperparathyroidism

A

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
Q

Secondary hyperparathyroidsim

A

Inc PTH, secondary to chronic disease

1) Chronic Reneal Failure
2) dietary deficiency of Vit D & C

hypercalcemia does not occur

82
Q

Tertiary hyperparatheyroidism

A

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
Q

Pseudohypoparathyroidism

A

inherited condition >

normal to elevated PTH

resistent to PTH in the proximal renal tubules

84
Q

Familial hypocalciuric hypercalcemia

A

Benign autosomal dominant condition

hypercalcemia/hypophos

Low Ca urine

mutation in calcium receptor of the parathyroid gland

85
Q

Hyperparathyroidism – s/s & treatment

A
  • 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
Q

hypoparathyroidsim

A
  • 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
87
Q

RAAS Pathway

A
88
Q

SIADH

A
  • 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
Q

DI

A
  • 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
Q

Hyperpituitarism

s/s

3 most common hormones & syndromes

Treatment

A
  • 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
Q

Primary Hypofunction of the Adrenal Cortex

A
  • 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
Q

Secondary Hypofunction of the Adrenal Cortex

A
  • Secondary hypercortisolism
    • prolonged administration of exogenous glucocorticoids, which suppress ACTH secretion. S/s similar to Addision, except NO hyperpigmentation
93
Q

Thyrotoxicosis

A

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
Q

Graves

A

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
Q

Hyperthyroidism – nodular thyroid disease

A
  • 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

96
Q

Thyrotoxic crisis (thyroid storm) – test question

A
  • 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
Q

Thymus

Hormone produced

funtion

Too little

A

Thymosin

T-lymphocytes development & production. Also train body to have self-response

too little: AI

98
Q

4 hypothroidsim primary reasons

A

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
99
Q

Secondary hypothyroidism

A
  • deficiency of hypothalamus/thyrotropin-releasing hormone (TRH) and pituitary/TSH
100
Q

Hypothyroidism - s/s & Treatment

A
  • 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
101
Q

Myxedema & Myxedema Coma

A

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

102
Q
A

Pathophysiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions