Anemia, Fever and Temp regulation Flashcards

1
Q

What is hemoglobin a measure of?

A

gm/dl; blood HB concentration

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2
Q

What is MCV?

A

average volume of red cells, mean corpuscular volume, volume of blood x HCT / #RBC

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3
Q

What is MCHC?

A

mean corpuscular hemoglobin concentration, HB/HCT,

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4
Q

What is reticulocyte count?

A

number of reticulocytes/total RBC;

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5
Q

What is hematocrit?

A

MCV x RBC, volume percent of RBC

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6
Q

What is mean corpuscular hemoglobin?

A

MCH, HB/RBC, concentration of hemoglobin packed in RBC

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7
Q

What is RDW?

A

red cell distribution width, measure variation in cell size, increased in sickle cell and nutritional deficiencies

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8
Q

What is anisocytosis?

A

RBC unequal size

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9
Q

What is poikilocytosis?

A

abnormally shaped

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10
Q

What is polychromasia?

A

abnormal increase in # of RBC premature in blood

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11
Q

what is hypochromia? How is this determined?

A

hypopigmentation; pale area more than 1/3 of RBC

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12
Q

What is microcytic? macrocytic? What cell is used for size comparison?

A

small RBC; large RBC; compare size to WBC

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13
Q

What is microcytic anemia?

A

Hb is decreased below normal and the MCV less than 80fl, MCHC may or may not be decreased if so hypochromic

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14
Q

What are the three general causes of microcytic anemia?

A

abnormality in iron metabolism, globin metabolism, and porphyrin metabolism

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15
Q

What are the causes of iron metabolism?

A

inadequate iron intake, chronic blood loss, and anemia of chronic disease

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16
Q

What are the causes of inadequate iron intake in microcytic anemia?

A

pediatric age, pregnant moms (iron uptake by fetus, suboptimal stores before pregnancy), otherwise inadequate iron intake in adults rare cause of microcytic anemia

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17
Q

What are the causes of chronic blood loss in microcytic anemia?

A

most common is GI; GI- ulcer, colon or gastric carcinoma, hiatal hernia, esophageal varices, ulcerative colitis, crohn disease, leiomyoma, salicylate, meckel diverticulum, hookworm, angiodysplasia; Female gential- dysfunctional uterine bleed, endometrial hyperplasia/carcinoma, excessive menses; Pulmonary- carcinoma, chronic infection; Urinary- bladder cancer, chronic infection

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18
Q

What are the causes of anemia of chronic disease? what amount are microcytic? normocytic?

A

rheumatoid arthiritis and other autoimmune disorders, cancer, chronic infection, severe tissue injury; 30% micro, 70% normo

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19
Q

What are the reasons for anemia of chronic disease?

A

impaired Fe flow into RBC- hepcidin triggers degrade. iron exporter (ferroportin) thus limiting egress from enterocytes and macrophages (limits Fe for microorganisms), may lead to anemia- infection, malignancy, and inflammation; decreased RBC survival, insufficient erythropoietin to stimulate RBC production

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20
Q

What are the types of thalassemia’s?

A

inherited, heterogeneous group, alpha and beta chain most common, in minor not anemia but have microcytosis, major= severe anemia

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21
Q

What are the features of Hemeglobin E?

A

SE Asia, most common globin abnormality, HgbS, beta chain abnormality, homo (marked hypochromia, microcytosis with little or no anemia) and heterozygous

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22
Q

What us serum ferritin? Decreased means? What can falsely increase?

A

principle storage form of iron; decrease in iron stores; chronic disease, when acute phase reactant increases (surgery, febrile illness, liver cell necrosis), oral or parenteral iron administration

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23
Q

What is iron-binding capacity?

A

IBC is a reflection of transferrin levels, although transferrin can be directly measured

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24
Q

What are causes of normocytic anemia?

A

chronic disease (most common), acute blood loss, marrow replacement (myeloplastic anemia), aplastic anemia, renal failure, hemolytic anemia

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25
Q

What are the causes of increased reticulocyte count in normocytic anemia? normal or decreased reticulocyte count?

A

acute blood loss, hemolytic anemia; anemia of chronic disease, renal failure, aplastic anemia, myelophthisic anemia (marrow replacement by infiltrative disease such as cancer and histoplasmosis)

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26
Q

What are the features of folate or B12 deficiency causing megaloblastic anemia?

A

maturation pattern in bone marrow, nuclear:cytoplasmic dyssynchrony, especially in RBC series, lab assessmentbegins with folate and B12 levels depending on hist and PE, schilling test- abnormal in B12 deficiency

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27
Q

what are the causes of drug-induced perturbed DNA synthesis?

A

antineoplastics, immunosuppressive, and antiretroviral

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28
Q

What are the causes of non-megaloblastic macrocytic anemia?

A

liver disease, hypothyroidism, bone marrow regeneration following blood loss or hemolysis with increased reticulocyte counts, myelophthisic anemia, myeloproliferative disease, multiple myeoloma, some causes of sideroblastic anemia

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29
Q

what neural structures are involved in thermoregulation? Which is the “thermostat”?

A

hypothalamus and limbic -> <- spinal cord and sympathetic ganglia; hypothalamus (esp. preoptic region, thermosensitive neurons)

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30
Q

What are mechanisms of heat production in the body?

A

mitochondrial oxidative phosphorylation (ADP->ATP, >50%), skeletal muscles during exercise ~25%, shivering in adult humans, and brown adipose tissue

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31
Q

where is brown adipose tissue located? characteristics? physiological role?

A

esp. near neck and scapulae; brown, profuse vasculature, numerous mitochondria (uncoupling protein 1, UCP1), thermoregulation in newborns and small mammals, possibly energy metabolism in adults (BAT activity inversely related to BMI)

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32
Q

What is the function of UCP1 in brown fat?

A

leaky inner membrane, energy released as heat, not stored as ATP, regulated by T3 locally

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33
Q

How is brown fat activated?

A

adrenergic neuron to B3 adrenergic receptor-> cAMP-> nucleus-> increase UCP1 production-> increase in heat

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34
Q

Where is heat lost? percent for each site?

A

skin 80-90%, 10% from lung

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35
Q

What is the mechanism for fine adjustment of temperature from hypothalamus?

A

sense absolute and change in temp of blood, autonomic nerves to skin BV, inc. BV diameter-> inc. heat loss -> dec. body temp OR dec. BV diameter-> dec. heat loss-> inc. body temp

36
Q

What is the mechanism for coarse adjustment of temperature from hypothalamus?

A

thermal skin receptors relay to hypothalamus which relays signals; autonomic neurons-> sweating-> dec. body temp OR somatic neurons-> shivering-> inc. body temp

37
Q

What causes hyperthermia? other name and clinical features?

A

abnormal thermoregulation; heat stroke- warm dry skin, no sweat, inc. temp, delirium, coma, organ failure, cardiac arrhythmia, death

38
Q

treatment for hyperthermia? risk groups?

A

rehydration, immersion in cool bath, not antipyretics; s/p CVA, cord injury, low mobility, low sweating (drugs or skin disorder), and diuretics

39
Q

what is normal body temp? What is the upper limits of normal?

A

old- 37C and 98.6F; new- 36.8C or 98.2F (men 98.1, women 98.4), 37.7C or 99.9F

40
Q

What are some things that cause normal body temperature variation? slight elevation?

A

normal diurnal variation (circadian T rhythm,0.5C -0.9F, high point 4-6p, low point 2-6a); menstruation, 1st trimester, ovulation, giant meal, hard exercise (1-4 deg), ambient temp >85F)

41
Q

what are the bodies high->low gradients? Regional variants of temp?

A

core-> epidermis, thrunk-> extremeties, hand-> fingertips, flexor->extensor surface; heart, brain and GI-37, scrotum 32, fingertips 20-25

42
Q

How does regional body temp effect infections?

A

mycobacterium leprae grow best at ~31C (affects ears, nose, fingers and toes), sporothrix grows best at 25C (affects extremities, rarely organs, heat to treat), rhinovirus grows best at 33C (temp of nasopharynx

43
Q

How does regional temp variation effect rash development?

A

some spread warm to cool (trunk to extremities, i.e. VZV) some spread cool to warm (extremities to trunk, i.e. rickettsia rickettsi)

44
Q

What are exogenous pyrogens? How do they work?

A

microbes or their products, ligands for TLR, stimulate cells to make endogenous pyrogens (macrophage, monocyte, PMNs, glial cells, neurons

45
Q

What are endogenous pyrogens? How do they work?

A

cytokines (IL-1beta, IL6, TNF alpha, IFN gamma), work at hypothalamic level- increase cyclooxygenase which increases PGEs-> reset thermostat higher

46
Q

what role does PGE2 play in fever?

A

levels high in hypothal and 3rd ventricle, highest near circumventricular organs (network of large capillaries, pyrogen-> endothelial rxn= 1st step), triggers release cAMP-> induces release of monoamine NT, hypotalmic reset up, causes myalgia, arthralgia in peripheral tissues

47
Q

What are endogenous cryogens? Examples?

A

affect firing of thermosensitive neurons (help control upper limit of body T), arginine vasopressin, alpha-MSH, neurochem (epi and NE), glucocorticoids and their inducers (CRF, ACTH)

48
Q

What are acute phase proteins? What effects change in levels?

A

rise or fall by 25%, altered due to production by hepatocytes; substantial- infection, trauma, surgery, burns, tissue infarction, inflammatory states; moderate- hard exercise, heatstroke, and childbirth; small- psychological stress and psychiatric illness

49
Q

What are some examples of acute phase proteins?

A

C-reactive protein, amyloid A, haptoglobin, fibrinogen, and procalcitonin

50
Q

What are some other acute phase reactions?

A

neuroendocrine, hematopoietic, and metabolic

51
Q

What does CRP bind and do?

A

binds phosphocholine on B and to pahgocytes, activates complement

52
Q

What is amyloid A, it binds to and does what?

A

apolipoproteins that bind lipoproteins, inc. adhesion and chemotaxis of phagocytes, ?inflammation in coronary arteries?, 2ndary amyloidosis if chronic

53
Q

What is haptoglobin? What does it do?

A

anti-inflammatory antioxidant, aids wound healing

54
Q

What is fibrinogen? What does it do?

A

coagulation component, affects rate of RBC fall in plasma (erythrocyte sedmentation rate, ESR, or sed rate)

55
Q

What is procalcitonin? What does it do?

A

prohormone (thyroid C cell response to hypercalcemia), inc. w/ B infection (IL1-beta), rises faster than ESR or CRP, falls quick if infection responds to Rx, no increase if viral (PCT sytnh. inhibited by IFN-gamma), biomarker for respiratory infection

56
Q

What occurs in the neuroendocrine acute phase response?

A

inc. CRH, ACTH and corticol; inc. adrenal secretion of catecholamines

57
Q

What occurs in the hematopoietic acute phase response?

A

anemia of chronic disease, leukocytosis, thrombocytosis

58
Q

What occurs in the metabolic acute phase response?

A

dec. muscle and negative nitrogen balance, dec. gluconeogenesis

59
Q

what are the benefits of fever?

A

preserved thru evolution (all vertebrates and some invertebrate), prevent fever (inc. death in animals), high temps inihibit B growth (Rx syphilis and gonorrhea), associated cytokines can aid host defense

60
Q

What are some harmful effects of fever?

A

seizures (103F or 40C, infants and young kids, prob rate of rise, high fever any age ~105), increased metabolic demands (dec. LV stroke volume and work), loss of brain function (>106F or 41C any age)

61
Q

What is the host perspective on fever? species perspective?

A

effect either good or bad; mediates speedy recovery from mild-moderate infection and hastens death of hopelessly infected who pose epidemiologic threat

62
Q

When and with what do you treat fever?

A

controversial- probly ok; high fever in very young (prevent seizures or metabolis demands too great; ASA (avoid under 21-Reye’s), acetaminophen, NSAIDS- inhibit COX-> dec. PGE2, 4-6hrs round the clock; steroids- inhibit CO and mRNA for cytokine synthesis

63
Q

What is the cause and treatment of intermittent fever?

A

pyogenic abcess, prn ASA; 2 daily spikes- military TB, GC endocarditis, salmonellosis, malaria, visceral leishmaniasis (Kala azar)

64
Q

What are some causes of recurrent fever (cycle of fever and afebrile) days? weeks?

A

malaria, meningiococemia, cholangitis, dengue f., yellow f., Colorado tick f., relapsing f. (borrelia) and influenza; Hodgkins disease (pel-ebstein fever), brucellosis, relapsing F. (Borrelia), ocassionally TB

65
Q

What are some general features of drug fever?

A

common cause, only sign of drug rxn in 3-5%, increased risk w/ more drugs taken (esp. elderly), increased risk w/ HIV

66
Q

What are the mechanisms of drug fever?

A

hypersensitivity, altered thermoregulatory mechanisms, directly related to administration, related to pharmacologic effect, idiosyncratic reactions

67
Q

What are the features of drug fever due to hypersensitivity?

A

most common, Ag-Ab complex formation, T-cell response, usually in 3 days, but up to years, may see: rash, uticaria, mucosal ulcers, liver, kidney, lung, bone marrow dysfunction

68
Q

What are the features of drug fever due to altered thermoregulation?

A

exogenous thyroid hormone (inc. metabolic rate-> inc heat production), anticholinergics (dec. sweating-> dec. heat loss), and sympathomimetics (inc. vasoconstriction-> dec. heat loss; amphetamine and cocaine)

69
Q

What are the features of drug fever due to drug administration?

A

IV fluid contaminated with endotoxin, chemical phlebitis, local inflammation at injection site, low-grade fever after vaccines, intrinsic pyrogenic prop. (amphotericin B, bleomycin)

70
Q

What are the features of drug fever due to pharmacologic effect?

A

chemotherapy (dying cells pyrogens-> cytokine release; Jarish-Herxheimer rxn (Antibiotic rxn-> dead bugs-> induce cytokines), may see rash, symptoms worse (syphilis, brucellosis, enteric fever)

71
Q

What are the idiosyncratic rxns that cause drug fever?

A

malignant hyperthermia, neuroleptic malignant syndrome (NMS), serotonin syndrome, glucose-6-phosphate dehydrogenase deficiency

72
Q

What are the features of malignant hyperthermia?

A

(rare), T >40C, muscle rigidity, metabolic acidosis, and BP instability, occurs during anesthesia (halothalene, succinylcholine), autosomal dominant in 50%, mutation in ryanodine receptor (Ca channel in skeletal muscle SR)

73
Q

What are the features of NMS?

A

high fever, muscle rigidity, altered mental state and dysautonomia (BP up and down), >25 drugs (all deplete CNS dopamine), major tranqs (haloperidol), significant mortality, RX: DC drug, dantrolene, bromocriptine

74
Q

what are the features of serotonin syndrome?

A

agitation, hyperthermia, diaphoresis, tachycardia, rigidity (similar to NMS), inc. stimulation of 5HT1A receptors (SSRI meds, inc. risk if given with linezolid), also LSD, lithium, L-dopa, and MAO-inhibitors

75
Q

What are the features of drug fever with G-6-PD deficiency?

A

fever with: primaquine, quinine sulfate and sulfonamides, hemolytic anemia is more worrisome

76
Q

What is fever of unknown origin? setting?

A

> 38C (101F) every day or repeatedly, 3wk duration (eliminates self-limited cause), no Dx after > 2 visits or 3d in hospital; community, clinic, or hospital

77
Q

What are the leading causes of fever of unknown origin?

A

infection (30-40%), Neoplasm (20-30%), collagen or vascular (10-15%), granulomatous (5-10%), Misc (10-20%), and unknown (10-15%)- SQ fecal injection to induce, etc

78
Q

What infections are a leading cause of FUO?

A

occult abscesses, TB, endocarditis, CMV

79
Q

What neoplasms are a leading cause of FUO?

A

leukemia, lymphoma, myeloma, hyerpnephroma, and hepatoma

80
Q

What collagen or vascular conditions are a leading cause of FUO?

A

SLE, RA, rheumatic fever, arteritis

81
Q

What granulomatous diseases are a leading cause of FUO?

A

sarcoidosis, granulomatous hepatitis, IBD

82
Q

What are the miscellaneous leading causes of FUO?

A

drug, PE, thermoregulatory disorder, endocrine disorder (hyperthyroid, Addison’s, pheochromocytoma), factitious/fraudulent

83
Q

What are the common causes of nosocomial FUO?

A

hospital acquired infections, post-op complications, and drug fever

84
Q

What are the common causes of FUO in cancer or transplant patient?

A

majority infection!, cause documented in only 50%

85
Q

What are the common causes of FUO in HIV or AIDS patient?

A

HIV primary infection, mycobacterial (TB or NTM esp MAI), CMV- toxoplasmosis, lymphoma