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1
Q

Hormones secreted by the anterior pituitary

A

ACTH, thyroid stimulating hormone (TSH), LH, FSH, prolactin, growth hormone, and melanocyte stimulating hormone (MSH)

2
Q

Hormones secreted by the posterior pituitary

A

Vasopressin (ADH), oxytocin

3
Q

Disorder of too much ADH

A

SIADH

  • Hyponatremic
  • hyperosmolarity
  • hypervolemia/ wt gain
4
Q

Disorder of too little ADH

A

DI

  • Polyuria, polydipsia
  • UOP 8-12 L/day (norm 1-2)
  • low urine specific gravity
  • low urine osmolarity
  • hypernatremia
5
Q

Too much GH

A

Gigantism- kids and adolescents

Acromegaly- adulthood

6
Q

Hypofunction of pituitary gland

A
  • Panhypotituitarism (all hormones affected)
  • ACTH deficiency- cortisol deficiency
  • TSH deficiency-altered metabolism
  • FSH and LH deficiency- lack of secondary sex characteristics
  • GH deficiency- lack of growth in children
7
Q

DM type 1

A

Polyuria, polydipsia, polyphagia
Weight loss, fatigue
-Pancreatic atrophy and loss of beta cell function, no longer producing insulin

8
Q

DM type 2

A

Cells become insulin resistant

-fatigue, recurrent infections, visual changes, s/s of neuropathy

9
Q

Signs of hypoglycemia

A

tachycardia, palpitations, diaphoresis, tremors, pallor, arousal anxiety

10
Q

DKA

A

Polyuria, dehydration, kussmal respirations, sweet/fruity breath, glucose over 250, acidotic, urine ketones
-usually associated with type 1

11
Q

HHS

A
  • emergency
  • precipitated by infections, noncompliance of meds, usually type 2 DM
  • glycosuria, polyuria, dehydration, coma
  • glucose over 600
12
Q

Somogyi effect

A

hypoglycemia with rebound hyperglycemia

  • usually type 1 and kids
  • eat a high protein snack at night to prevent hypoglycemia
13
Q

Dawn phenomenon

A

early morning glucose elevation without nocturnal hypoglycemia
-increase nighttime insulin dose to peak during the morning

14
Q

Microvascular complications of DM

A

retinopathy, neuropathy, and nephropathy

15
Q

Macrovascular complications of DM

A

CAD, CVA, PAD, infection

16
Q

Hyperparathyroid

A
  • increase in pth levels

- hypercalcemia, hyperphosphatemia, pathologic fractures

17
Q

Hypoparathyroid

A
  • decrease in pth levels

- hypocalcemia, hypophosphatemia, muscle spasms, chvostek’s sign (cheek), and trousseau sign (BP cuff)

18
Q

Addison’s disease

A

adrenal insufficiency; low cortisol levels, elevated ACTH

-weakness, hyperpigmentation, vitiligo

19
Q

Cushing’s

A

too much ACTH leads to excessive cortisol levels
-truncal (central) obesity, moon face, buffalo hump, na/h20 retention, glucose intolerance, purple striae, brown hyperpigmentation of skin

20
Q

Thyrotoxicosis

A

hyperthyroidism

-low TSH and high T3 and T4

21
Q

Grave’s disease

A

hyperthyroidism
-increased metabolic rate, tachycardia, heat intolerance, weight loss, insomnia, palpitations, diarrhea, goiter, exopthalmus

22
Q

Thyrotoxic storm

A

rare and life threatening

  • results from excessive stress, increased T3 and T4
  • hyperthermia, tachycardia- esp atrial tachydysrhythmias, high output heart failure, delirium, nvd
23
Q

Hypothyroidism

A
  • primary is iodine deficiency (most common worldwide)
  • autoimmune thyroiditis (most common in US)
  • congenital
  • thyroid carcinoma
  • secondary hypothyroidism
24
Q

Hypothyroidism (cont.)

A
  • low basal metabolic rate, cold intolerance, lethargy, lower body temp, possible diastolic hypertension
  • myexedema: non-pitting edema esp around eyes, hands, and feet, thickening of tongue
25
Q

Myxedema coma

A
  • emergency

- diminished LOC, hypothermia without shivering, tachypnea, hypotension, hypolgycemia, lactic acidosis, coma

26
Q

Chromosomes

A

carries genetic information; 23 pairs of chromosomes

27
Q

Genes

A

tells body how to make proteins; responsible for inherited characteristics

28
Q

Allele

A

one of the possible forms of a gene (2 possible forms are dominant and recessive)

29
Q

Codon

A

a set of three adjacent nucleotides or a triplet that constitutes the genetic code for a particular amino acid that is to be added to a polypeptide chain in the synthesis of a protein

30
Q

Autosome

A

22 chromosome pairs in both males and females; not sex (X and Y)

31
Q

Genotype

A

the set of genes in our DNA that is responsible for a particular trait

32
Q

Phenotype

A

the physical characteristics of a trait

33
Q

Hemizygous

A

males, having only one X chromosome, are said to be hemizygous for genes on this chromosome.
-females are homozygous because they have 2 X chromosomes

34
Q

Transcription

A

the process of making an RNA copy of a DNA molecule

-gene splicing occurs (cleans it up to get ready for translation)

35
Q

Translation

A

RNA is decoded in a ribosome (site of protein synthesis) to produce a specific amino acid chain, or polypeptide.

36
Q

DNA

A

Cytosine (C), thymine (T), adenine (A), guanine (G)

A to T, C to G

37
Q

RNA

A

Cytosine (C), uracil (U), adenine (A), guanine (G)

A to U, C to G

38
Q

Mutation

A

any inherited alteration of genetic material

39
Q

Mutagens

A

are agents, such as radiation and chemicals, that increase the frequency of mutations

40
Q

Autosomal recessive inheritance

A

two copies of an abnormal gene must be present in order for the disease or trait to develop

41
Q

Turner syndrome

A

females only have one X chromosome

  • absence of ovaries
  • short stature
  • webbing of the neck
  • widely spaced nipples
42
Q

Klinefelter syndrome

A

Individuals with at least one Y and two X chromosomes

  • male appearance, gynecomastia, small testes, sparse body hair
  • treat with testosterone
  • likelihood of disorder increases with mother’s age
43
Q

Down syndrome

A

Trisomy 21

  • mental challenges, low nasal bridge, epicathal folds, protruding tongue, flat/low set ears, poor muscle tone
  • increased risk for congenital heart disease, respiratory infections, and leukemia
44
Q

Genetics of common diseases

A

CAD, htn, DM

45
Q

Alzheimer disease

A

produces amyloid plaques and neurofibrillary tangles

-risk doubles if you have a first-degree relative

46
Q

Alcoholism

A

risk is 3-5x higher in the individual with an alcoholic parent
-adoption studies- studies show it runs in genes rather than caregiver/environment

47
Q

Schizophrenia

A

recurrence risk among offspring of one affected parent is 10x higher than the gen population

48
Q

Bipolar affective disorder

A

also called manic depressive disorder

  • risk rises 5-10% in an individual who has an affected first-degree relative as compared to normal, which is 0.5%
  • genes that affect serotonin, dopamine, and noradrenaline systems have been implicated
49
Q

Dominance and recessiveness

A

If two alleles are found together, then the allele that is observable is dominant and the one whose effects are hidden is recessive

50
Q

Carrier

A

Has a disease allele but is phenotypically normal; can pass disease to offspring

51
Q

Autosomal aneuploidy

A

Aneuploidy is a somatic cell that does not contain a multiple of 23 chromosomes.

  • Trisomy: cell contains 3 copies of one chromosome
  • Monosomy: presence of only 1 copy of any chromosome (is often fatal)
52
Q

Deletions

A

chromosome breakage or loss of DNA

-ex: cri du chat syndrome; “cry of the cat”-low birth weight, mentally challenged, and microcephaly

53
Q

Duplications

A

excess genetic material; usually have less serious complications

54
Q

Inversion

A

chromosomal rearrangement in which a chromosome segment is inverted
-ABCDEFG becomes ABEDCFG

55
Q

Translocation

A

the interchange of genetic material between nonhomologous chromosomes

56
Q

Fragile sites

A

chromosome develops breaks and gaps when the cells are cultured in a folate-deficient medium

57
Q

Congenital malformations

A

congenital diseases present at birth; having other disorders along with the congenital disease is common

58
Q

Concordant traits

A

both members of a twin pair share a trait;

more genetic

59
Q

Discordant traits

A

A twin pair does not share a trait;

more environmental

60
Q

Polygenic trait s

A

effects of multiple genes cause the variations in traits

-focus is on the genes- usually many (poly) genes

61
Q

Multifactoral traits

A

environmental factors cause the variations in traits

62
Q

Quantitative traits

A

are measured on a continuous numeric scale

follows a normal bell curve for distribution

63
Q

Incidence Rate

A

the number of new cases of a disease reported during a specific period (typically 1 year) divided by the number of individuals in the population

64
Q

Prevalence Rate

A

the proportion of the population affected by a disease at a specific point in time; varies from population to population

65
Q

Epigenetics

A

are chemical modifications of DNA sequences that alter the expression of genes, resulting in disease and phenotypic variations

66
Q

DNA methylation

A

makes part of the gene silent or inactive

67
Q

Genomic imprinting

A

the process of gene silencing, in which genes are predictably silenced, depending on which parent transmits them

68
Q

Prader-Willi

A

inherited from dad

  • abnormal pairs of the long arm of chromosome 15
  • short stature, hypotonia, small hands/feet, obesity, mild mental retardation, hypogonadism
69
Q

Angleman syndrome

A

Same deletion of pairs from long arm of chromosome 15 as prader willi, but angleman is inherited from mom*
-severe mental retardation, seizures, ataxic gait

70
Q

Beckwith-Weidemann syndrome

A

overgrowth condition accompanied by an increased predisposition to cancer

  • large for gestational age, neonatal hypoglycemia, large tongue
  • uniparent disomy, affecting chromosome 11
71
Q

Russel-silver syndrome

A

undergrowth condition

-growth retardation, proportionate short stature, leg length discrepancy, small/triangular shaped face

72
Q

Layers of epidermis (from outermost to innermost)

A
  • stratum corneum
  • stratum lucidum
  • stratum granulosm
  • stratum spinosum
  • stratum basale
73
Q

Langerhans cell

A
  • migrate from epidermis to bone marrow
  • immune defense against environmental triggers
  • present antigens to T cells
74
Q

Merkel cells

A
  • touch receptors on epidermis

- identifies stress occurring on skin

75
Q

Keratinocytes

A
  • produce keratin

- promotes hydration of skin

76
Q

what is the dermis composed of?

A

elastin
collagen
reticulum
gel-like ground substance connective tissue

77
Q

Layers of the dermis

A

Papillary- hair follicles, sebaceous and sweat glands, blood/lymph vessels, mast cells (release histamine), macrophages

Reticular- histocytes and fibroblasts that help with wound healing

78
Q

Eccrine sweat glands

A
  • in dermis
  • thermoregulators through evaporation
  • palms, soles, forehead
79
Q

Apocrine sweat glands

A
  • stink!

- scalp, axilla, genitalia, face, abd

80
Q

Hypodermis

A
  • deep, fatty layer of skin
  • adipocytes and connective tissue
  • veins and arteries run through this layer
81
Q

Staging pressure ulcers

A
  1. nonblanchable
  2. partial; epidermis and/or dermis
  3. full thickness: subcutaneous
  4. full thickness; muscle, bone
82
Q

atopic dermatitis

A

*eczema
severe pruritus- hallmark sign
eczematoid appearance with redness, edema, and scaling

83
Q

where does atopic dermatitis appear in infants?

A

scaly red lesions appear on face, scalp, trunk, extensor surfaces of arms/legs

84
Q

where does atopic dermatitis appear in children and adults?

A

neck, AC and popliteal fossa, hands, feet

85
Q

chronic eczema

A
  • thick, leathery, hyperpigmented skin

- lichenification

86
Q

stasis dermatitis occurs as a result of?

A

venous stasis
edema
vascular trauma

87
Q

stasis dermatitis sequence of events

A
edema
erythema
pruritus
scaling
petechiae
hyperpigmentation
ulcerations
88
Q

seborrheic dermatitis involves what areas of the body?

is it constant or intermittent?

A
-chronic skin inflammation involving:
scalp
eyebrows
eyelids
nasolabial folds
axillae
chest
back

-periods of remission/exacerbation

89
Q

seborrheic dermatitis in infants

A

“cradle cap”

90
Q

psoriasis

A
  • T cell autoimmune mediated skin disease
  • cells do not have time to mature or keratinize
  • systemic: arthritis and CV disease
91
Q

Lichen planus

A
  • benign self limiting inflammatory disorder
  • more prevalent during spring/fall
  • may be linked to Hep C
92
Q

manifestations of Lichen Planus

A
  • nonscaling flat papular violet-colored lesion
  • pruritus on wrists, ankles, lower legs, and ginitals
  • oral=white lacy rings
93
Q

acne vulgaris

A
  • inflammatory disease of pilosebaceous follicles

- hypertrophy of sebaceous glands and telangiectasia

94
Q

acne rosacea

A

chronic immune mediated skin inflammation

easily exacerbated

95
Q

acne rosacea manifestations

A
  • telangiectasia

- rhinophyma (bulbous nose)

96
Q

folliculitis

A

infection of hair follicles
S. aureus
pustules with erythema

97
Q

furuncle

A

*boil
inflammation from preceding folliculitis
follicular wall into surrounding dermis
S. aureus, MRSA

98
Q

carbuncle

A

collection of infected hair follicles
abscess can develop
erythematous, painful, drainage

99
Q

cellulitis definition, cause?

A

infection in dermis/subcutaneous

staphylococcus or GBS, MRSA

100
Q

erysipelas definition, cause?

A

superficial cellulitis
acute infection of upper dermis
streptococcus pyrogenes
face, ears, lower legs

101
Q

tinea cruris

A

jock itch
inner and upper surface of thighs
scaling vesicular patches, defined border

102
Q

tinea manus

A

hand
dry, scaly, erythematous OR moist vesicular lesions
clusters, intense itching

103
Q

HSV 1

A

infected saliva

cold sores/fever blisters

104
Q

HSV 2

A

genital infections
skin to skin contact during viral shedding
mother to neonate; high mortality

105
Q

varicella and herpes zoster
what kind of virus?
where does infection occur?

A

DNA virus
infection occurs within keratinocytes
contact, airborne precautions

106
Q

verrucae
cause?
transmission?

A

*warts
caused by HPV
transmitted by touch

107
Q

manifestations of verrucae

A

rough, grayish surface

108
Q

condylomate acuminata

A

venereal warts
sexually transmitted, highly contagious
oncogenic HPV primary cause of cervical cancer

109
Q

condylomate acuminata

A

veneral warts- very contagious
sexually transmitted
cauliflower like lesions

110
Q

kwashiorkor

A

protein deficient
1-4 years of age weaned from breast milk to high starch
can have leaky guy, inflammation, store fat in liver, pancreatic atrophy

111
Q

marasmus

A

deficient in all nutrients (protein, carbs)
younger than 1 year old
stunned growth, muscle/fat wasting, anemia, diarrhea, dermatosis, low Hgb

112
Q

gastrin

A

“stimulates secretion of gastric juice”
enhances relaxation of stomach
enhance peristalsis of stomach

113
Q

cholecystokinin

A

stimulates digestion of fat and protein

114
Q

D cells

A

somatostatin- inhibitory
decreases release of glucagon/insulin
slows gastric motility/perstalsis

115
Q

Kupffer cells

A

phagocytic cells

central to innate immunity

116
Q

stellate cells

A

remove foreign substances from blood

trap bacteria

117
Q

pit cells

A

natural killer cells

interferon y- tumor defense

118
Q

what stimulates pepsin?

what inactivates it?

A

acetylcholine stimulates

alkaline environment of duodenum inactivates

119
Q

what is saliva composed of?

A
water with mucous
sodium bicarb
potassium
chloride
salivary amylase

has IgA

120
Q

acute liver failure patho

A

hepatocytes become edematous, patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma
*hepatic necrosis irreversible

121
Q

acute liver failure s/s

A

anorexia, N/V, abd. pain, progressive jaundice

122
Q

consequences of portal HTN

A

varices
splenomegaly
hepatopulmonary syndrome

123
Q

MCC of ascites

A

cirrhosis

124
Q

hepatitis

A

autoimmune or viral inflammation of the liver

125
Q

phases of hepatitis

A

Prodromal: 2 weeks post exposure to jaundice
Icteric: jaundice phase
Recovery: when jaundice resolves

126
Q

manifestations of cirrhosis

A

nausea, anorexia, fever, abd pain, jaundice

127
Q

cirrhosis patho

A
  • irreversible inflammatory fibrotic disease that disrupts liver function
  • biliary channels blocked, causes portal HTN
128
Q

biliary cirrhosis

A
  • begins in bile canaliculi and ducts
  • primary: autoimmune- T lymphocyte mediated
  • secondary: obstruction
129
Q

black pigmented cholelithiasis

A

form in gallbladder

chronic liver and hemolytic disease

130
Q

brown pigmented cholelithiasis

A

bacterial infection in bile ducts

bili stasis or bili parasites EW!

131
Q

manifestations of cholecystitis

A

inflamed gallbladder

- fever, leukocytosis, rebound tender, abd guarding

132
Q

pancreatitis patho

A
  • damage to pancreatic cells and ducts that causes a leakage of pancreatic enzymes into pancreatic tissues
  • the enzymes can leak into blood and cause injury to blood vessels and other organs
133
Q

chronic pancreatitis patho and manifestations

A
  • destroyed acinar cells and islets of Langerhans
  • pancreatic parenchyma destroyed
  • s/s: may have continuous or intermittent abd pain
134
Q

intussusception

A
  • telescoping or invagination of one part of the intestine to another
  • MCC: ileum into cecum
135
Q

intussusception s/s

A
  • abd pain
  • vomiting soon after pain
  • “currant jelly” stools (dark and gelatinous)
  • infants: sausage shaped mass, colicky, flexes knees
136
Q

Hirschsprung disease

A
  • obstruction of colon

- failure of neural crest cells to migrate to GI tract: “skipped segments”

137
Q

Hirschsprung disease manifestations

A

delayed meconium, poor feeding, poor weight gain, abd distention

138
Q

lower airways: pulmonary anatomy

A

trachea** who knew?!
bronchi
bronchioles

139
Q

carina

A

ridge where trachea divides into R and L bronchi

140
Q

hila

A

where R and L bronchi enters lungs

blood and lymph vessels

141
Q

goblet cells

A

produce mucous

142
Q

surfactant

A

lipoprotein that coats the inner surface of the alveolus

decreases surface tension which prevents collapse

143
Q

left shift oxyhgb dissociation curve

A
  • Hgb increased affinity for O2
  • alkalosis
  • hypothermia
  • hypocapnia (hyperventilation)
144
Q

right shift oxyhgb dissociation curve

A
  • Hgb decreased affinity for O2
  • acidosis
  • hyperthermia
  • hypercapnia (hypoventilation)
145
Q

emphysema patho

A
  • abnormal permanent enlargement of the gas exchange airways
  • destruction of alveolar walls without obvious fibrosis
  • loss of elastic recoil
146
Q

primary emphysema?

secondary?

A

primary- deficiency of a1- antitrypsin

secondary- cigs, air pollution, childhood resp. infections

147
Q

emphysema manifestations

A
  • thin
  • dyspnea on exertion (may progress)
  • little cough, little sputum
  • tachypnea w prolonged expiration
  • barrel chest
  • tripod position
148
Q

Laryngotracheobronchitis
who?
when?

A

*croup
6 mo-3 years old
late autumn/winter

149
Q

causes of Laryngotracheobronchitis

A

commonly caused by a virus

  • parainfluenza
  • influenza A
  • RSV
150
Q

manifestations of Laryngotracheobronchitis

A
usually after episode of rhinorrhea
sore throat
fever
seal like barking cough
hoarse voice 
inspiratory stridor
151
Q

pulmonary edema patho?

MCC?

A
  • excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability
  • MCC- L heart fail
152
Q

early asthmatic response

A

IgE causes mast cells to degranulate, releasing a large # of inflammatory mediators

  • vasodilation
  • increased cap. permeability
  • bronchial smooth muscle contraction
  • mucosal edema
153
Q

ARDS patho and manifestations

A

alveoli fill with fluid

  • massive pulmonary inflammation
  • increased cap. permeability
  • pulmonary edema
  • shunting
  • V/Q mismatching
  • hypoxemia
154
Q

manifestations of atelectasis

A

dyspnea
cough
fever
leukocytosis

155
Q

posterior pituitary- ADH

A

ADH

  • controls plasma osmolality (ADH released when increased)
  • causes water reabsorption in the kidneys
156
Q

too much ADH

A
SIADH
hyponatremia
hypoosmolality
urine hyperosmolality
hypervolemia
157
Q

too little ADH

A

DI (neuro, nephro, dipsogenic)

  • inability of kidney to increase permeability to water
  • 3 P’s
  • inability to concentrate urine