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sophomore year slump > patho test 3 > Flashcards

patho test 3 Flashcards

1
Q

Disorders of kidney development

A

10% of people born with potentially significant malformations can be a result of hereditary influences, most often acquired defect during development

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2
Q

renal agenesis

A

complete failure of kidney development
bilateral: incompatible with life (stillborn, die early after birth)
unilateral: more common, typically compensensatory or hypertrophy

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3
Q

renal hypoplasia

A

kidneys are small in size, unilateral usually, discovered incidentally (usually hypertension)
Bilateral- progressive renal failure

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4
Q

renal dysplasia

A

can effect all or part of the kidney
multicystic kidney disorder: risk of hypertension and Wilms tumors. Annual follow ups with blood pressure and sonograms

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5
Q

cystic diseases of the disease of the kidney

A

can be single or multiple
Vary in size
Symptomatic or asymptomatic
Acquired or usually heredity

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6
Q

Autosomal dominant polycystic kidney disease

A

most common inherited kidney disease
multiple expanding cysts
destroy kidney structure and cause renal failure
manifestations: pain, hematuria, UTI’s and Hypertension (diagnosed with ct scans)
supportive care: control pain, UTI’s, and BP

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7
Q

autosomal recessive polycystic kidney disease

A

childhood kidney disease, present at birth with rapid progressive into kidney failure
bilateral flank masses
severe renal failure
impaired lung development
hypertension
75% will die before a month old

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8
Q

nephronophthisis

A

small kidneys
multiple cysts
usually juvinile
progresses to chronic kidney disease
polyuria
polydipsia (excessive thirst)
enuresis (bed wedding)

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9
Q

medullary cystic kidney disease

A

small kidney
adult onset
chronic kidney disease
polyuria
polydipsia
enuresis

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10
Q

acute nephrotic syndrome

A

acute inflammatory process
can be post infectious or secondary to systemic diseases such as lupus
s&s: sudden onset of hematuria, proteinuria, decreased glomerular filtration rate, oliguria, edema, hypertension

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11
Q

acute post infectious glomerulonephritis

A

occurs after infections with certain strains of group A beta hemolytic streptococci, 7-10 days post-infection
common in underprivileged nations
S&S: oliguria, hematuria, edema (in the face and hands), hypertension
treatment: antibiotics, supportive care

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12
Q

acute pyelonephritis

A

etiology: bacterial infection (usually E coli)
uncomplicated: no structural abnormality
complicated: structural abnormalities
acute onset: shaking, chills, fevers, constant ache in the loin and back area. Usually unilateral
treatment: antibiotics 10-14 days

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13
Q

renal failure

A

kidneys fail to remove metabolic end products from the blood and regulate the fluid, electrolyte and pH balance of the extracellular fluid, could be caused by renal disease, systemic disease or urologic defect from a non renal origin

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14
Q

acute kidney injury

A

abrupt onset, often reversible if caught early
abrupt decline (within 48 hours) in kidney function, fluid and electrolyte balance
mortality rate between 25-80 depending on cause
increase creatinine and reduction in urine production
can be caused by decreased blood flow without ischemic injury
ischemic, toxic, obstructive
classified prerenal, intrarenal, post renal (prerenal and intrarenal most common)
diagnosed by: BUN 8-20, creatinine <1.2, urine analysis, renal ultrasound, kidney biopsy
S&S: decreased urine output, fluid retention, edema, pulmonary congestion, hypertension
untreated: neuromuscular irritability, intense drowsiness, coma, death

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15
Q

chronic kidney disease

A

develops over the course of time, irreparable damage, can lead to the need of dialysis

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16
Q

prerenal injury (aki)

A

most common
marked decrease in renal blood flow
can be reversed if cause for ischemia can be corrected fast
causes: hemorrhage, impaired perfusion due to CHF, cardiogenic shock, anaphylaxis, sepsis, IV contrast, ace inhibitors, angiotensin receptor blockers, anti inflammatories
elderly most at risk

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17
Q

intrarenal kidney injury (aki)

A

damage to the kidney itself
Ex: infections, glomerulonephritis, DM, nephrotoxic substances

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18
Q

post renal injury (aki)

A

results from obstruction of urine outflow from the kidneys
Ex: calculi, strictures, bladder tumors, BPH (most common)
Treat the cause of the obstruction

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19
Q

immunity

A

protection from infectious disease

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20
Q

immune response

A

collective coordinated response of cells and molecules of the immune system

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21
Q

innate immunity

A

natural immunity, early rapid response
developed by secretions of mediators
opsonins: bind to and tag microorganisms for more efficient recognition
cytokinin: regulate activity of other cells, amplify inflammation, initiation of the adaptive immune response
phagocytic lymphocytes: early response followed by macrophages
dendrites: from bone marrow, link innate and adaptive
nk cells: recognize infected and stressed cells respond by killing cells

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22
Q

adaptive immunity

A

specific or acquired immunity, less rapid but more effective
focused response to specific foreign agent
distinguishes between microbes and molecules to remember pathogens quickly and produces a heightened immune response on subsequent encounters with the same agent
composed of lymphocytes and their products
humoral and cell mediated immunity

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23
Q

macrophages

A

mature form of monocytes, located in most tissues, engulf and kill invading organisms, dispose of pathogens and infected cells, antigen-presenting cells for adaptive immunity (long lived)

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24
Q

granulocytes

A

short lived, neutrophils, basophils, eosinophils

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25
Q

lymphocytes

A

b lymphocytes produce antibodies, mediate humoral immunity
t cell lymphocytes cell mediated immunity
T helper cells: help b lymphocytes produce antibodies

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26
Q

central lymphoid tissue

A

bone marrow, thymus- immune cell production and maturation

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27
Q

peripheral lymphoid tissue

A

lymph nodes: remove lymph, filter foreign material before it goes back to the blood, and center for proliferation and response of immune cells

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28
Q

spleen

A

left abdominal cavity, filters antigens from the blood, important in response to systemic infections

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29
Q

innate immune system consists of

A

epithelial layer: physical and chemical barriers between internal and external environments- epidermis, keratin, salty acidic environment, antibacterial proteins
phagocytic neutrophils
macrophages
dendritic cells

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30
Q

complement system

A

primary effector system for innate and adaptive systems
consists of protein activated microbed and promote inflammation and destruction of microbes

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31
Q

classical pathway of microbe recognition

A

adaptive immunity, recognizes antibody bound to surface of microbe or structure

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32
Q

lecitin pathway of microbe recognition

A

innate pathway uses plasma protein (mannose binding ligand) binds to residue

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33
Q

alternative pathway of microbe recognition

A

innate pathway, recognizes certain microbial molecules

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34
Q

lining of the respiratory, GI, and urogenital tracts

A

Mucus traps and washes away microorganisms
cillia: move microbes trapped in mucus to throat where it is coughed or sneezed out

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35
Q

antigens (adaptive immunity)

A

aka immunogens stimulate an immune response
Ex: bacteria, fungi, virus, protozoa, parasites
Non microbial antigens: pollen, poison ivy, insect venom, transplanted organs
recognized by receptors on immune cells and cause antibodies to be formed

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36
Q

t lymphocytes

A

Helper t cells: trigger immune response and are essential for differentiation of b cells into antibody producing cells
Regulatory T cells
Cytotoxic t cells

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37
Q

Antigen presenting cells

A

macrphages and dendritic cells that process and present antigen peptides to helper t cells

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38
Q

Cell surface major histocompatibility complex molecules (MHC)

A

key recognition molecules the immune system uses to distinguish self from nonself
Class one: present in all nucleated cells other than those of the immune system, interact with CD8+ T cells in the destruction of cells affected by intracellular pathogens or cancer
Class two: found on antigen presenting cells and b lymphocytes, aid in cell communication

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39
Q

humoral immunity (adaptive immunity)

A

protection from b lymphocytes: eliminates extracellular microbes and microbial toxins
primary tissue response: antigen first introduced into the body
latent period before detection of the antibody
activation takes one to two weeks but can be several weeks before it is detectable
secondary (memory response): occurs on second or subsequent exposure to antigen. rise in antibodies and occurs quicker due to memory cells. Ex: booster shots

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40
Q

immunoglobulins

A

IgG: placenta
Ig A: breast milk
IgM
IgD
IgE: allergies

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41
Q

Passive Immunity

A

immunity transferred through another source
Ex: crosses placenta in mother baby in utero or through breastmilk, transferred from other period or animals

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42
Q

self regulation of immune response

A

inadequate response can lead to immunodeficiency
excessive or inappropriate response can lead to allergic reactions or autoimmune disease
tolerance: inhibition of an immune response, non reactive to self antigens while producing immunity to foreign agents, can lead to inability to respond to infectious agents

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43
Q

newborns

A

protected by maternal antigens (IgG and IgA), a lot of IgG crosses in the last few weeks of pregnancy which makes preemie babies so immunodeficiency, HIV moms will pass HIV antibodies to baby, but may not transfer virus

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44
Q

aging

A

elderly have changes in immune response and are more susceptible to infections
more autoimmune and immune complex disorders
higher incidence of cancer and less response to vaccines

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45
Q

inflammatory response results from cellular injury that ruptures cells

A

trauma
environmental irritants
microorganisms
free radical damage
hypoxia
surgery

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46
Q

inflammation

A

prepates injured area for healing
leukocytes (neutrophils and macrophages) remove debris and provide growth factors
nutrients (proteins, glucose, vitamins) provide the building flocks for cells
clotting factors and platelets limit damage

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47
Q

plasma protein system

A

clotting cascade to prevent further bleeding. Kinin cascade produces bradykinin which causes pain, vasodilation, and vascular permeability. Complement cascade stimulates opsonins, chemotaxic factors, and anaphylatoxins which causes release of histamine
the vascular response: histamine and bradykinin stimulate vasodilation. increased blood flow causes heat, redness, pain and edema
cellular response: chemotaxis factors attract neutrophils to move to move to the capillary walls (migrate), phagocytosis

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48
Q

inflammatory response

A

reaction to tissue damage caused by injury or infection
redness, heat, pain, swelling, loss of function
fever: caused by endogenous pyrogens, prodromal, chill, defervescence stage (sweating)

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49
Q

exudate (drainage)

A

serous: watery, plasma like
fibrinous: clotted
serosanguinous: blood tinged
sanguineous: blood
suppurative/purulent: pus

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50
Q

chronic inflammation

A

continuous exposure to irritants
could result in granuloma formation, giant cell formation, cancers

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51
Q

stages of wound healing

A

inflammation: 1-2 days
proliferation and new tissue formation: 2-8 weeks for maximum strength, may involve regeneration and resolution, repair with scar tissue, but loss of function
remodeling and maturation: up to two years

52
Q

factors affecting wound healing

A

oxygenation: reduced in COPD and atherosclerosis
circulation: reduced in elderly, CHF, DM, MI
Hydration: reduced in illness, hydration and age
Age: accelerated in young and reduced in the elderly
Immunity: reduced in HIV, stress, infection
Medications: cortisone, chemotherapy, immunomodulators

53
Q

Types of wound healing

A

first intention: must be clean, able to approximate wound edges, fasted and preferred
second intention: used in contaminated wounds, large amount of tissue lost, very slow, large scare
third intention: rarely used, to close large wounds that are cleaned enough (skin grafting)

54
Q

wound healing process

A

macrophages dissolve clots, clear debris add TGF-B (transforming growth factor beta) to stimulate collagen precursor to procollagen
VEGE (vascular endothelial growth factor) stimulates angiogenesis
MMP (matrix metalloproteinases) remodel collagen and fibrin
collagen lattice forms, granulation tissue fills in wound, hypertrophic scar tissue overfills wound. Cicatrization (maturation) may take 1-2 years. Collagen contracts and the scar tissue becomes lighter and smoother

55
Q

dysfunctional healing

A

wounds may fail to close or may re-open due to poor wound healing conditions
non-union: failure to adherence
dehiscence: wound edges separate, expose underlying tissues
evisceration: underlying viscera are exposed
wounds may become infected
abscess: a walls pocket of infection
sinus tract: a narrow tunnel forms
cellulitis
necrosis and gangrene may occur
fibrin or dysfunctional collagen synthesis
fistula formation
adhesions
contractures
strictures
keloids

56
Q

systemic markers of vascular inflammation

A

homocysteine level: elevated in reduced folate levels, b vitamins, riboflavin inhibits increased endothelial damage in arteries
C-reactive protein: increases to neutralize inflammatory chemicals low risk for cardiovascular events
infectious agents found in plaques
endothelial dysfunctions: lack of nitrous oxide

57
Q

atherosclerosis

A

condition in which fatty deposits called plaque builds up on the inner walls of the arteries

58
Q

COPD: emphysema

A

pathophysiology: chronic stretching of the alveoli due to obstruction of the bronchial passageways which prevents easy expulsion of gases causing a decrease in alveolar elasticity, causes a dead space in the lung tissue
barrel chest, pink puffer
increases risk of right side heart failure , fluid retention, pneumonia
these patienrs tend to adapt to the condition by increasing quantity of RBC’s altering the pigmentation of their skin resulting in them being referred to as pink puffer

59
Q

hypersensitivity disorders

A

Disorders caused by immune response
type one: immediate hypersensitivity disorders: IgE mediated, begin rapidly, allergic reactions, cytokinins secreted differentiate B cells into IgE which act as growth factors for mast cells and activate eosinophils
Primary or immediate phase response, vasodilation, vascular leakage, smooth muscle contraction
Secondary or late phase: intense infiltration of tissues with eosinophils and other acute or inflammatory cells, epithelial cell damage, leukotrienes, and prostaglandins produce response
type two: antibody mediated disorders
Type three: immune complex mediated disorders
type four: cell mediated disorders

60
Q

type one hypersensitivity: anaphylactic reaction

A

Life threatening- can occur within minutes of exposure
Characterized by widespread edema, difficulty breathing, vascular shock secondary to vasodilation
Results from antigen introduced by injection- insect sting, or absorption across skin, GI mucosa
Level of severity depends on level of sensitization
Treatment- airway, IV, epinephrine- relaxes bronchoconstriction, increases BP
Pt should have epi-pen, family members should be trained, medi-alert bracelet

61
Q

Type I Hypersensitivity: Local (Atopic) Reactions

A

Confined to specific site by exposure
Atopic-genetically determined hypersensitivity to common allergens
Mediated by igE- mast cell reaction
Most common disorders- hives, allergic rhinitis (hayfever), atopic dermatitis, food allergies and some forms of asthma

62
Q

Type I Hypersensitivity: Allergic Rhinitis

A

Characterized by sneezing, itching, and watery discharge from nose and eyes (rhinoconjunctivitis), can also be associated with sinusitis and bronchial asthma
Severe attacks: general malaise, fatigue, muscle soreness, and HA
Typical allergens: pollen from ragweed, grasses, tress and weeds, fungal spores, house dust and mites, animal dander and feather
Diagnosis: skin ,serum or nasal smear (increase eosinophils)
Treatment: antihistamines, topical and oral decongestants, desensitization

63
Q

Type I Hypersensitivity: Food Allergies

A

Any food can trigger- most common are milk, eggs, peanuts, tree nuts, seafood, cooking food may change symptoms
Acute response (hives and anaphylaxis), Chronic (asthma, atopic dermatitis and GI disorders)
Can occur at any age, but usually childhood

64
Q

Type II Hypersensitivity

A

Mediated by IgG or IgM antibodies directed against antigens on cell surfaces or connective tissue
Antigens can be endogenous or exogenous (drug metabolites)
3 types of Type II Complement and antibody mediated destruction- mismatch blood transfusion rx, hemolytic dx of newborn due to ABO or rH incompatibility or drugs (HIT)
Complement and antibody mediated inflammation-glomerulonephritis
Antibody- mediated dysfunction- changes cell function Graves dx (TSH receptors), MG (ACE receptors)

65
Q

Type III Immune complex-Mediated Disorders

A

Complement- and Antibody-Mediated Cell Destruction
Involve formation and deposition of insoluble antigen-antibody complexes
Responsible for vasculitis (SLE), systemic immune complex disease (serum sickness) and local immune complex disease

66
Q

Type IV Cell- mediated Hypersensitivity

A

Direct cell cytotoxicity- sensitized CD8+T cells kill antigen-bearing target cells
Delayed-type hypersensitivity reactions- presensitized CD4+T cells release cytokines that damage and kill antigen-containing cells- tuberculin skin test
Allergic contact dermatitis- inflammatory response after sensitized- cosmetics, hair dyes, topical drugs- erythematous, popular and vesicular lesion, pruritus and weeping 12-24 hours post exposure, lasts days to weeks treatment with corticosteroid creams
Hypersensitivity Pneumonitis- exposed to inhaled organic dusts or occupational antigens; labored breathing, dry cough, chills, fever, headache, chronic exposure may lead to chronic lung disease with little reversibility

67
Q

Transplantation

A

Taking cells, tissues or organs (graft) from on individual (donor) to another (recipient)
Rejection is a major barrier to transplantation- recipients immune system recognizes the graft as foreign and attacks it.
Hyperacute rejection: occurs almost immediately after transplantation, caused by existing recipient antibodies and initiate type III Arthus- type sensitivity
Acute rejection- occurs within first few weeks or months Chronic rejection occurs over prolonged period, caused by T-cell cytokines that damage BV causing ischemic damage to graft tissue

68
Q

Graft-versus-host disease (GVHD)

A

Occurs most often in bone marrow transplants patients
3 things must occur:
The transplant must have a functional cellular immune component
The recipient tissue must bear antigens foreign to donor tissue
Recipient immunity must be compromised to the point that cannot destroy transplanted cell
Occurs most often in bone marrow transplants patients
3 things must occur:
The transplant must have a functional cellular immune component
The recipient tissue must bear antigens foreign to donor tissue
Recipient immunity must be compromised to the point that cannot destroy transplanted cells

69
Q

Autoimmune Disease

A

Disruption in self-tolerance that results in damage to body tissues by immune system
Self-tolerance is maintained through central and peripheral mechanisms that delete autoreactive B or T cells that suppress or inactivate immune responses that destroy host cells, defects in this mechanism predispose to autoimmune disease
May be triggered by environmental stimuli, infections, genetic predisposition
Treatment based on tissue involved, immunosuppressive drugs, steroids

70
Q

Immunodeficiency disorders

A

10 Warning Signs of primary Immunodeficiency
4 or more new ear infections in 1 year
2 or more serious infections in 1 year
2 or more months on antibiotics with little effect
2 or more PNA within 1 yearFailure of infant to gain weight or grow normally
Recurrent deep skin or organ abscess
Persistant thrush, fungal infections of skinNeed for IV ABX
2 or more deep seated infections including septicemia
Family Hx

71
Q

Acquired Immunodeficiency Syndrome

A

Profound immunosuppression
Transmitted blood or body fluids that contain the virus, sexual contact is the most frequent mode*Destroys CD4 cells
3 phases:
Primary phase: shortly after infection- mono like symptoms
Latency phase: may last for years
Overt phase decrease in CD4 count
Treatment involves drugs that interrupt replication of virus- no cure
Treat opportunistic infections
Diagnosis: ELISA- enzyme-linked immunosorbent assay
Western blot if ELISA is +, the western blot can identify false-positive EIA results
Home tests

72
Q

Pregnancy and HIV

A

Women infected with HIV and transmit to offspring in utero, labor or breast milk
HIV antibody can be present in babies from the mother, uninfected babies is usually disappears within 18 months

73
Q

Glands of the Endocrine System

A

Pituitary
Thyroid
Parathyroid
Adrenal glands

74
Q

Organs that also produce hormones

A

Pancreas
Gonads
Hypothalamus

75
Q

Hormones

A

Regulate water and electrolytes
Respond to adverse conditions such as infection, trauma, stress
Help with growth and development
Reproduction
Pregnancy maintenance
Digestion
Nutrient storage
Endocrine hormones can exert various effects on various organs
Ex. Estradiol

76
Q

Paracrine

A

Hormone produces action locally on other cells

77
Q

Autocrine

A

Produces action on the cells from which they were produced

78
Q

Hypothalamic Hormone

A

Synthesis and release of Anterior Pituitary Hormones are regulated by releasing or inhibiting hormones from the hypothalamus
Hypothalamus hormones that regulate secretion of anterior pituitary hormones
GH-releasing hormone (GHRH)
Somatostatin
TRH
Corticotropin releasing hormone (CRH)
Gonadatropin releasing hormone (GH)

79
Q

Regulation of Hormone Levels

A

Hypothalamus activity is regulated by negative feedback mechanism
TSH–> T3T4

80
Q

Pituitary gland (master gland)

A

pea shaped hormone locates at the base of the brain

81
Q

Pituitary gland- anterior lobe (adenohypophysis, glandular tissue)

A

Thyrotrophs-produce TSH
corticotrophs- produce corticotropin (ACTH)
Gonadotrophs - produce gonadotrophins (LH, FSH)
Somatrophs- produce GH
Lactotophs- produce prolactin

82
Q

Pituitary gland- posterior lobe: neurohypophysis neural tissue

A

stores and releases: antidiuretic hormone (ADH) and oxytocin
Both of these hormones are synthesized in the hypothalamus

83
Q

hypofunction

A

Congenital defect: gland/enzyme
Gland destroyed: blood flow, infection, inflammation, autoimmune response, neoplasm
Age, atrophy due to drug
Receptor defect

84
Q

hyperfunction

A

Excessive hormone production
Excess stimulation
Hyperplasia
Hormone producing tumor
Drugs (steroids/cushings)

85
Q

Altered endocrine: primary disorder

A

orignate in the target gland for producing the hormone

86
Q

altered endocrine: secondary diagnosis

A

target gland function is normal but altered by defective levels of stimulating or releasing hormones from the pituitary gland. Ex thyroidectomy- eliminates TSH stimulation

87
Q

altered endocrine: tertiary disorders

A

results form hypothalamic dysfunction- both pituitary and target glands are under stimulated

88
Q

hyperpituitarism

A

typical cause pituitary adenoma (benign tumor from anterior pituitary)
Less common cause: hyperplasia, carcinoma of the anterior pituitary, secretion of hormones by extra-pituitary tumors, hypothalamic lesions
Lactotrophic Tumors are most frequent
Small benign tumors composed of prolactin secreting cells causing hyperprolactinemia
In women: inhibit LH causing amenorrhea, galactorrhea, infertility
In men: ED and loss of libido

89
Q

hypopituitarism

A

Decreased secretion of pituitary hormones causing hypofunction of the secondary organs- 70-90% of anterior pituitary must be destroyed to become evidence
Causes: congenital, acquired abnormalities that destroy anterior pituitary, deficiency of hypothalamic hormones, lesions
Gradual progressive loss- loss of GH, LH, FSH then eventual loss of TSH, ACTH*Maybe be manifested R/T hormone- GH loss decreased growth in children, decreased libio, ED, amenorrhea, then Hypothyroid

90
Q

Growth hormone disorders

A

Growth hormone (somatotropin): essential for growth and aids in metabolic functions

Growth patterns are measured over time and is related to parent height as well

91
Q

idiopathic short stature

A

normal variant of short statue with unk own cause, 2 or more SD below age group

92
Q

psychosocial dwarfism

A

functional hypopituitarism, seen in some emotionally deprived children: poor growth, potbelly, poor eating and drinking habits

93
Q

Classic growth hormone deficiency

A

Decreased lean mass, increased fat mass, hyperlipidemia, decreased bone mineral density, reduced exercise capacity and diminished sense of well-being

Associated with- increase central adiposity, insulin resistance, dyslipidemia (metabolic syndrome), elevated CRP

94
Q

Giantism

A

growth hormone excess before puberty, usually by somatotrophe adenoma

95
Q

Acromegaly

A

GH excess in adulthood

96
Q

Precocious Puberty

A

Early activation of hypothalamic pituitary gonadal axis
Occurs before 6 in African American girls, 7 in Caucasian girls and 9 in boys of both races
Development of secondary sex characteristics and fertility
Tall stature in childhood and short stature in adulthood

97
Q

Thyroid Gland

A

Body’s largest single organ specialized in hormone production
Thyroid hormone secretion regulated by the hypo-thalamic-pituitary-thyroid feedback
Thyroid hormone increases metabolism and protein synthesis
Thyroid Function Tests: T3, T4, TSH

98
Q

hypothyroidism

A

General slowing down of the metabolic process
Most often caused by Hashimoto Thyroiditis-autoimmune disorder than can destroy the thyroid gland
Manifestations: gradual onset of generalized weakness, weight gain despite decrease appetite, cold intolerance, dry sterm-127kin, coarse, brittle hair, puffy face
Diagnosis: elevated TSH, low T4 (primary)*Treatment: levothyroxine( synthroid)

99
Q

myxedema

A

non-pitting edema- especially face
Myxedema coma: life-threatening , end stage hypothyroidism, coma, hypothermia, cardiovascular collapse, hypoventilation, hyponatremia, hypoglycemia and lactic acidosis
Treatment: aggressive supportive therapy i.e. cardiovascular, electrolytes, warming blanket

100
Q

hyperthyroidism

A

High levels of thyroid hormone
Due to hyperactive thyroid gland- graves disease, goiter
Manifestations: nervousness, irritability, weight loss, tachycardia, palpitatins, SOB, excessive sweating, heat intolerance, exophthalmos
Treatment- radioactive iodine to eradicate thyroid gland, surgery, antithyroid drugs- PTU, methimazole, and drugs to control symptoms- Beta-Blockers

101
Q

thyroid storm

A

Life-threatening thyrotoxicosis- rare now because of good diagnosis tools
Caused when hyperthyroid is not adequately treated, precipitated by stress, infection, DKA, trauma or manipulation of the hyper active thyroid during thyroidectomy
Manifested: Very high fever, tachycardia, CHF, angina. Agitation, restlessness, and delirium- high mortality rate
Treatment- should be rapid- cooling w/o shiver response, fluids, glucose, steroids, PTU, methimazole, BB, NO ASA- increases levels of free thyroid hormones

102
Q

Primary Cortical Insufficiency

A

Addison’s Disease- (rare) adrenal cortical hormones are deficient, ACTH levels are elevated because of lack of feedback
Autoimmune destruction of the adrenal cortex, before 1950’s TB was the major cause, metastatic CA, CMV, hemochromatosis
Manifestations: urinary loss of sodium, chloride and H2O, decrease loss of K+, decreased Cardiac output, hyperkalemia, orthostatic hypotension, dehydration, weakness and fatigue
Treatment- fludrocortisone, hydrocortisone

103
Q

Acute Adrenal Crisis

A

Life-threatening, can be caused by illness in someone with Addison’s disease
Manifestations- N/V, muscular weakness, hypotension, dehydration, and vascular collapse
Treatment- fluids both NS and D5W, glucocorticoid replacement therapy

104
Q

Cushing Syndrome

A

Hypercortisolism from any cause
Manifesations- protruding abdomen, subclavicular fat pads, buffalo hump on back, moon face, weakness and thin extremities
Treatment- remove or correct the cause of hypercortisolism

105
Q

Diabetes

A

The body primarily metabolizes glucose and fatty acids for energy
The brain does not produce or store glucose, but needs it exclusively for function
Tissues obtain glucose from the blood
Liver stores excess glucose as glycogen, and uses gluconeogenesis to convert amino acids, lactate and glycerol into glucose during fasting or when glucose intake does not keep up with demand
Blood glucose levels reflect the difference liver released glucose and the amount of glucose removed from blood by body tissues
Fats can be used for fuel during fasting or diabetes mellitus- the breakdown makes fatty acids that are converted to ketones in the liver (not converted to glucose)
Energy metabolism is controlled by several hormones: insulin, glucagon, epinephrine, GH and glucocorticoids
Insulin is the only hormone that controls blood glucose levels
Insulin facilitates the transport of glucose into body cells, decreases livers production and release of glucose into the bloodstream
Insulin decrease lipolysis and the use of the fats as fuel
Glucagon and epinephrine promote glycogenolysis
Glucagon and glucocorticoids increase gluconeogenesis

106
Q

Diabetes Mellitus Type 1

A

Type I- beta-cell destruction, absolute insulin deficiency
Type 1A- immune mediated destruction of beta-cells (90%)
Occurs more commonly in children and adolescents
Genetic predisposition, environmental triggers, infection, and T-lymphocyte- mediated hypersensitivity
Type 1B-idiopathic
Strongly inherited
African americans and Asian

107
Q

Categories of Risk for Diabetes

A

Fasting glucose levels- plasma glucose levels after 8 hrs of fasting
< 100 mg/dl nml
100-125 mg/dl impaired fasting glucose (pre-diabetes)
>126 mg/dl provisional diabetes
Oral Glucose Tolerance Test- measures bodies ability to remove glucose from the body within 2 hrs after consuming 75g on glucose 300ml of water
<140mg/dl nml
140-199 mg/dl impaired (prediabetes)
> 200 provisional diabetes
HGA1C> 6.5 diabetes

108
Q

Diabetes Mellitus Type 2

A

Type II- insulin resistance, relative insulin deficiency
Relative insulin deficiency
90% of Diabetes casesOlder and overweight, recently obese children
Metabolic abnormalities- insulin resistance, increased glucose production by liver, impaired insulin secretion by pancreatic beta- cells
Increased postprandial blood glucose levels
Genetic, behavioral, environmental factor leads to diabetes
Family history twofold-fourfold increased riskObesity, inactivity
Visceral obesity leads to increased postprandial glucose levels
Metabolic syndrome (syndrome X, insulin resistance): hyperglycemia, hypertriglyceridemia, low HDL, high LDL, elevated CRP

109
Q

Diabetes detection

A

Type 1 rapid onset
Type 2 gradual usually detected through incidentsl blood tey
3 P’sPolyuria
Polyphagia
Polydipsia
Weight-loss (type I)
FBG<100
Casual or random blood glucose > 200mg/dl with 3P’s, and blurred vision
OGTT after 2hr >200mg/dl
HgA1c- >6.5

110
Q

Diabetes Management

A

Exercise (especially type 2)
Sulfonyurea’s (glipizide), meglitinides (repaglinide), biguinides (metformin), alpha-glucosidase inhibitors (acarbose), Incretin- based agents (exanatide), Insulin

111
Q

Diabetes Complications: Diabetic Ketoacidosis

A

hyperglycemia, metabolic acidosis, acute life-threatening complication of uncontrolled DM
Usually affects Type 1, but can affect Type 2 (sepsis, severe trauma)
Lethargy, vomiting, abdominal pain, coma, fruity breath
Blood glucose levels > 250mg/dl
Low bicarbonate mild (15-18mmol/L, ph 7.25-7.3); moderate (10-<15 mmol/l, ph 7.00-7.24), severe (<10mmol/L, ph <7.0)
Leads to dehydration and electrolyte imbalance
Goal of treatment- hydration, treat metabolic and electrolyte imbalances- insulins by infusion

112
Q

Hypoglycemia

A

Insulin reaction resulting from excess insulin, below normal blood glucose levels
Occurs most often in patients taking insulin, sulfonylurea
Over dose of insulin
Failure to eat
Exercise
Decreased need for insulin (decreased stress, meds)
Rapid onset-anxiety, tremors, tachycardia, cool clammy skin, incoherent, coma seizures- some people may have decreased reaction
Treatment- juice, candy, glucagon

113
Q

Over Dosage of Insulin

A

Somogyi Effect: hypoglycemia in pre-dawn hours 2-4am
rapid decrease in blood glucose during nighttime hours
stimulates release of hormones: cortisol, glucagon and epinephrine, to increase blood glucose by lipolysis, gluconeogenesis, and glycogenolysis
Monitor glucose between 2-4 am, reduce insulin dose at bedtime

114
Q

Hyperglycemia

A

Dawn Phenomenon: Hyperglycemia on awakening
Headache, sweats, nightmares
increase bedtime dose of insulin
Ketoacidosis: with inadequate amounts of insulin sugar can not be metabolized and fat catabolism occurs Extreme thirst, polyuria, fruity breath, kussmaul breathing, rapid thready pulse, dry mucous membranes, poor skin turgor, blood sugar level> 250mg/dl

115
Q

Chronic Complications of diabetes: Diabetic Neuropathies

A

paresthesia, numbness, tingling, impaired pain, decreased ankle and knee reflexes, ED

116
Q

Chronic Complications of diabetes: Diabetic Neuropathy

A

lesions that occur in the diabetic kidney, cause CKD- contributing factor- HTN, family history, smoking, HLD, poor glycemic control, increased urine albumin secretion >30mg/day

117
Q

Chronic Complications of diabetes: Diabetic Retinopathy

A

most frequent cause of new blindness, characterized by abnormal vascular permeability, mircro-aneurysm, hemorrhage, scarring, retinal detachment- poor glucose control, HTN. HLD- should have regular dilated eye exams

118
Q

Chronic Complications of Diabetes: Macrovascular complications

A

atherosclerosis, cerebral vascular disease, HTN, hyperglycemia, altered platelet formation, HLD- reduce risk factors

119
Q

Chronic Complications of Diabetes: Diabetic Foot Ulcers

A

effect of neuropathy and PVD, should have full foot exam yearly

120
Q

Chronic Complications of Diabetes: Infections

A

soft tissue, osteomyelitis, UTI, candida

121
Q

Stress response

A

activation of sympathetic nervous system, hypothalamic pituitary adrenal axis, immune system working to protect body from intense demands
Alarm stage- activation of sympathetic nervous system
Resistance stage- body selects most effective defense
Exhaustion- physiologic resources are depleted, and signs of systemic damage appear

122
Q

Adaptation

A

Individual has successfully created a balance between the stressor and the ability to deal with it
Affected by experience and previous learning, how fast it needs to occur, gender, age, health status, nutrition, sleep-wake cycles and psychosocial factors

123
Q

Stress

A

Stress response is designed to be self-limiting and protective
Prolonged activation of stress response because of overwhelming or chronic stressor can be damaging to health
Acute stress reaction and acute hyperglycemia are concerning in people with critical injuries or illness

124
Q

PTSD

A

Chronic activation of the stress response after experience that involved actual or threatened death or serious injury
S&S: states of intrusion (flashbacks),avoidance (emotional numbing), hyperarousal (intense activation of neuroendocrine system)

125
Q

Treatment for Stress

A

Avoid harmful coping behaviors
Progressive muscle relaxing techniques
Guided imagery
Music therapy
Massage therapy
Biofeedback

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