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finals Flashcards

1
Q

condensation of chromatin

A

Pyknosis

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2
Q

fragmentation of nucleus ‘nuclear dust’

A

Karyorrhexis

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3
Q

dissolution of nuclear structure as a result of enzymatic digestion

A

Karyolysis

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4
Q

localized death ofcells or tissues in a living organism

A

Necrosis

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5
Q

Programmedcelldeath (singlecells)

A

apoptosis

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6
Q

hypoxia(decrease amount of oxygen)

A

anoxia(no oxygen)

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7
Q

decrease in size ofcell

A

■ Atrophy:

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8
Q

refersto a branch of medical science that deals with tumors and cancers.

A

Oncology

“Onco” means mass or tumor, and “-logy” means study

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9
Q

—flat, smaller than 2 cm

A

• Macule (e.g., freckle)

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10
Q

—slightly elevated, smaller than 1 cm (e.g., eczema caused by allergy)

A

• Papule

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11
Q

—vesicle filled with pus (e.g., impetigo [bacterial infection])

A

• Pustule

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12
Q

—fluid-filled elevation of epidermis, smaller than 1 cm (e.g., herpesvirus lesion on the lip)

A

• Vesicle

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13
Q

—vesicle that measures more than 1 cm

A

Bulla (e.g., burns)

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14
Q

—superficial skin defect caused by scratching

A

Excoriation

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15
Q

• Four cardinal signs of inflammation (Celsus 30 BC-38 AD)

A 
• Heat (calor)
• Redness (rubor)
• Swelling (tumor)
• Pain (dolor)
-not included-Loss of function (function laesa - added later in 1900
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16
Q

• Five classical signs of inflammation

A
  • Swelling
  • Heat
  • Altered Function/Immobility
  • Redness
  • Pain
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17
Q
  • Fully differentiated B lymphocytes
  • Produce immunoglobulins (antibodies) (Ig)
  • Surface ofplasmacell is coated with Ig
A

• Plasmacells

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18
Q
  • Mature in thymus
  • Part of Cell-Mediated Immunity
  • 2/3rds of all lymphocytes in the blood, lymph nodesandspleen
  • All express protein CD3 on their membrane
  • Linked to T-cell receptor
  • Used to recognize antigens
A

T Lymphocytes

  • Several sub-types of T lymphocytes
  • T Helpercells
  • T Suppressorcells
  • Cytotoxiccells

• T helpercells(“master regulator”)
• Express proteinCD4 (aka CD4cells)
• 75% of all T-cells
• Assist B-cellsto matureandproduce antibody secreting protein mediators called lymphokines (ie. IL-1andinterferons)
• Activate macrophages – help to destroy bacteria
• Help other T-cellsrecognizeanddestroy virally infectedcells(CD8 = cytotoxic T-cells)
• Help NKcellskill infectedcells
• HIV destroys or inactivates helper T-cells, leaving the body at risk for infections

T Lymphocytes
• T suppressorcells
• Suppress activation of the immune systemandprevent pathologic self-reactivity (auto-immune disease)

• Cytotoxic Tcells
• Express CD8 antigen on their surface
• Mediate the killing of virus infectedcellsor tumorcells
• Clinical Conditions Affecting T-cells
• HIV
• Stress, Malnourishment
• Cancer, Diabetes
• Surgery
• Immunosuppressing drugs – corticosteroids
• Age – 65+ produce less Tcells
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19
Q

– inflammation dominated by pus

A

Purulentor suppurative

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20
Q
  • Acuteinfectious diseases:
  • – Palpable, tender, enlarged, fluctuant; if redandhot with a fever you’ll probably want to send them to their doctor
A
  • Chronicinfections:

* – Palpable, tender, enlarged; not usually red/warm

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21
Q

• What is the role of inflammatory chemicals such as histamine and bradykinin?

A
  • Histamine
  • Released by mastcellsandplatelets
  • Causes contraction of endothelialcellsof venules → gaps → increased blood vessel
  • permeability
  • Vasodilatorandbronchoconstrictor
  • Lasts less than 30 minutes

• Bradykinin
• Plasmaprotein formed by Hageman factor (Coagulation factor XII)
• Same effects ashistaminebut at a slower pace
Causes pain

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22
Q

• Know the types of skin cancers (based on their prognosis, which is least malignant versus most malignant?)

A
  • Seborrheic keratosis (“senile wart”)—most common epithelial skin tumor; benign
  • Basal cell carcinoma—most common malignant skin tumor; good prognosis
  • Squamous cell carcinoma—worst prognosis of tumors in this group; often preceded by actinic keratosis and carcinoma in situ
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23
Q

• Know the type of fungal infection (Tinea corporis, Tinea capitis, Tinea cruris, Tinea unguium)

A

• Tinea pedis or athlete’s foot - affects between toes

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24
Q

• The three basic cellular growth characteristics of neoplastic cells

A

Neoplastic Cells
• In contrast to tightly regulated cellgrowthin normal cells, tumor cells:

  1. Autonomous-Not under the control of body process, keeps dividing
  2. Excessive-Break the boundary of tissue and spread
  3. Disorganized- Cell division is random, no two look the same.
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25
Q

• Parasitic infestations and bites (Ticks, mites, fleas, lice – know the correct terminology for the skin disease for each)

A
  • Bites by blood-sucking insects – cause itchy papulomacular skin disease
  • Skin lesions are caused by substance injected by the insect
  • Fleas - typhus
  • Mosquitoes - malaria
  • Bed bugs
  • Lice – Pediculosis (head lice, body lice, pubic lice)
  • Ticks – Lyme disease
  • Sting of Bees and Wasps – allergies cause local reaction or anaphylactic shock
  • Scabies—contagious skin disease caused by Sarcoptes scabiei (mite), which burrow into the epidermis
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26
Q

• Overgrowth of pigment cells is the most common congenital skin developmental defects (Mongolian spot, port-wine stain/mark, strawberry hemangioma)

A

Birthmarks (Nevus)

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27
Q

• Has hereditary component (inherited Mendelian traits – autosomal dominant trait) • Child born covered with thick squames resembling fish scales)

A

• Ichthyosis congenital

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28
Q

• Generalized hypopigmentation due to an inborn error of metabolism • Unable to make melanin due to lack of enzyme tyrosinase • Increased risk of sunburns and skin cancer

A

• Albinism

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29
Q

Several skin disorders characterized by the formation of blisters on rubbing of the skin or minor trauma

A

• Epidermolysis bullosa •

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30
Q

are fungal pathogens that tend to live in “dead tissues” • Can cause the skin to itch and lead to secondary skin infections that lead to formation of fissures and scaling • Most common sites include the feet, head, nails, axilla and groin

A

Dermatophytoses

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31
Q

– chronic fungal infection of the nails

A

Onychomycosis

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32
Q

• An excess of hair

A

• Hirsutism (hormonal or idiopathic)

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33
Q

• Loss of hair from scalp

A

Alopecia •
• Alopecia areata - focal
• Diffuse alopecia (males > females)

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34
Q

Common disease of unknown origin affecting 1% to 2% of the population • Familial incidence • Slightly elevated papules and patches with scaling, mostly on extensor surface of knees and elbows but also the face and scalp

A

psoriasis

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35
Q

Generalized hypopigmentation due to an inborn error of metabolism • Unable to make melanin due to lack of enzyme tyrosinase • Increased risk of sunburns and skin cancer

A

• Albinism •

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36
Q

is a long-term skin condition characterized by patches of the skin losing their pigment. The patches of skin affected become white and usually have sharp margins. The hair from the skin may also become white. The inside of the mouth and nose may also be involved.

A

Vitiligo

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37
Q

• What is verruca vulgaris or wart?

A

Verruca vulgarisare commonwarts, which are caused by infection with human papillomavirus. Suchwartscan develop anywhere on the skin and frequently appear on the cuticle (the skin at the base of the nail) and sometimes the area beneath the nail.

38
Q

• Laceration – Sharp trauma involves disruption of the skin and the underlying blood vessels, caused by sharp objects such as knife or bullet

A

• Contusion – Blunt trauma caused by objects such as club or hammer; presents as a bruise

39
Q

• Burns – grading (least severe vs most severe)

A
  • First-degree burns • Erythema and swelling, transitory and reversible
  • Second-degree burns • Blisters involving the epidermis; hair follicles and adnexa in the dermis spared
  • Third-degree burns • Full-thickness burns with massive necrosis of epidermis and parts of dermis and hypodermis; cannot heal spontaneously
40
Q

– pathogenesis, symptoms, treatment
o Asthma −is a severe allergic reaction that occurs rapidly and causes a life-threatening response involving the whole body.
This reaction can lead to: difficulty breathing -Shock –Death
It is a severe response to an allergen leading to systemic histamine release causing:
systemic vasodilation bronchospasm,mucus & edema in airways and tissues

Triggers:
◦ bee sting ◦ Penicillin ◦ foods

Treatment: Administration of IM epinephrine  vasoconstriction

A

Type I: anaphylactic

Anaphylactic shock

41
Q

• Herpes virus infection (type 1 to 8 with example)

A 
• Type 1 (HSV 1)
• cold sores
• 70% population

• Type 2 (HSV 2)
• Genital
• 20% population
• birth canal infection
• Herpetic Whitlow (location) – terminal phalanx – HSV1 or 2
  • Type 3 - VaricellaZoster
  • 1 degree form:
  • highly contagious 1-2 days before vesicular rash
  • 2 degrees form: Herpes Zoster
  • 10- 20% reactivated
  • dermatome pattern

Type 4 – EBV (Epstein Barr virus)
• Infectious Mononucleosis - “the kissing disease”
• mucosal contact, lymph/blood spread
• 95% between 35-40years of age have been infected
• Fever, rash, fatigue, lymphadenopathy, spleen enlargement
• Possibly involved in later development of FM, CFS, and MS

Type 5
• Cytomegalovirus (CMV)
• 80%pop’nare carriers, esp. with AIDS
• transmission: all fluid except saliva, spread via lymphocytes
• usually asymptomatic/self-limiting
• In immunocompromised - fever, splenomegaly, hepatitis, blindness, peripheral neuropathy

Type 6 & 7 – B & T-cell viruses associated with
roseola (or 6th disease)
• Rash
• Fever
• Runny nose

Type 8 – associated withKarposi’ssarcoma in AIDS

42
Q

◦ Form of hyperthyroidism in women with antibody (Ab) against the TSH receptor on thyroid  goiter

A

o Grave’s disease

43
Q

◦ Severe muscle weakness

◦ Antibody (Ab) for Acetylcholine receptor on striated muscle

A

o Myasthenia gravis -

44
Q

is the most common type of autoimmunearthritis. It is caused when the immune system (the body’s defense system) is not working properly.

A

Rheumatoid arthritis(RA)
RA causes pain and swelling in the wrist and small joints of the hand and feet. Treatments for RA can stop joint pain and swelling.

45
Q

◦ Autoimmune disease of unknown origin ◦ Antigen is person’s own nucleus of cells ◦ Antinuclear antibodies (ANAs) which form complexes and deposit in varying organ systems
◦ Can affect any organ system ◦ Kidney disease, arthritis, skin disease (malar rash)
◦ Classic presentation is the triad of fatigue, joint pain and malar rash in women of childbearing age
◦ Dx by immunofluorescence microscopy

A

− Systemic lupus erythematous

46
Q

The infectious disease process includes the following components:

A

1) agent
(2) reservoir
(3) portals of entry and exit
(4) mode of transmission
(5) immunity. Types of agents range from the submicroscopic to the large parasites

47
Q

• What is candidiasis?

A

Candidiasisis a fungal infection caused by a yeast (a type of fungus) calledCandida. Some species ofCandidacan cause infection in people; the most common isCandidaalbicans.
Candidanormally lives on the skin and inside the body, in places such as the mouth, throat, gut, and vagina, without causing any problems

48
Q 
• Most numerous WBCs in blood (60-70%)
• First cells to appear in acute inflammation
• Features:
• Mobility
• Phagocytosis
• Bactericidal activity – kill bacteria
• Cytokine production – release mediators of inflammation
• Promote inflammation
• Recruit newleukocytes
• Cause symptoms of inflammation
A

• Polymorphonuclear Neutrophils (leukocytes)

49
Q
  • 2-3% of circulating WBCs
  • Appear 2-3 days After PMNs in area of inflammation
  • Longer lifespan – chronic inflammation
  • Like PMNs they are mobile, phagocytic and bactericidal
  • Interact with basophils
  • Allergic reactions– hay fever, asthma
  • Respond toparasitic infection(Mainly hellmas parasite, round worm, hook work and tape worm)
A

Eosinophils

50
Q
  • Less than 1% of circulating WBCs
  • Mostprominent in allergic reactions(IgE)
  • Cytoplasmic granules contain histamine
  • Precursors to Mast Cells
  • Basically basophils outside of the blood vessel
A

• Basophils

51
Q
  • Derived from monocytes in blood
  • Large
  • Appear at site of inflammation 3-4 days after onset of infection or injury
  • Long-lived
  • Chronic inflammation
  • Phagocytosis and release cytokines
A
  • Macrophages

* **two main phagocytic cells = Monocytes/Macrophages and Neutrophils”

52
Q

• Released from megakaryocytes in bone marrow
• No nucleus
• Cytoplasm contains vacuoles and granules
• Histamine, coagulation proteins, cytokines, growth factors
• Release histamine in early stages of inflammation
Lymphocytes and Plasma cells

A

Platelets (not cells, they are cellular fragments)

53
Q

is redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries. It occurs with any skin injury, infection, or inflammation.

A

Erythema(from the Greek erythros, meaning red)

54
Q

is a pale color of the skin that can becausedby illness, emotional shock or stress, stimulant use, or anemia, and is the result of a reduced amount of oxyhaemoglobin and may also be visible aspallorof the conjunctivae of the eyes on physical examination

A

Pallor

55
Q

refers to a bluish cast to the skin and mucous membranes.

It’s usuallycausedby low oxygen levels in the red blood cells or problems getting oxygenated blood to your body

A

Cyanosis

56
Q

is caused by a buildup ofbilirubin, a waste material, in the blood.

A

Jaundice-
An inflamed liver or obstructed bile duct can lead to jaundice, as well as other underlying conditions. Symptoms include a yellow tinge to the skin and whites of the eyes, dark urine, and itchiness

57
Q

Staphylococcus
• Most common bacterial pathogens on theskin
• Over 30 spp. – only a few relevant ones

• S. aureusisthe most virulent
• Leading causeofnosocomial( hospitalinfection) and community acquiredinfections
• 13%ofall hospitalinfections = 2 million/year leading to 60,000-80,000 deaths per year
• All ages
• Blood,skin, lung, soft tissue, joints, bones
• Gram +

A

S. aureus
• Transmission:
• Direct contact – nasal passages most common; also skin, axilla, perineum, vagina, oropharynx
• Risks:
• Insulin-dependantDiabetics; HIV+;hemodialysis; IV drugs; chronic skin lesions; corticosteroid use; surgery; burns
• Pathogenesis:
• Secretes membrane-damaging enzymes & toxins
• Stimulate a strong host immune response

Clinical pictureofS. aureus
• Clinical Manifestations:
• suppuration(pus) andabscess formation
• eg.Boils, pus filled vesicles
• respiratory tractinfection(esp. innewborns), osteomyelitis,infectionsofburns and surgical wounds,septicemia, Toxic Shock Syndrome, bacterial arthritis, bacterial endocarditis, impetigo
• ConsumptionofS.aureustoxins incontaminated foodiscommon causeoffood poisoning– Fever, chills, and diffuse erythema, pain, swelling

S. aureus
• Diagnosis: culture from infected site, blood, or other fluids
• Must test for antibiotic resistance
• Prognosis: good withtx, unless MRSA
• if untreated systemic (e.g. endocarditis)
• MRSA

58
Q 
• Most common in children, 5-10 y. old
• Incubation: 1-5 days
• Clinical Manifestations:
• sore throat with pain on swallowing,
• beefy red pharynx,
• tonsillar exudates,
• swollen tonsils and uvula,
• swollen regional lymph nodes,
• malaise and weakness,
• anorexia
• Can also colonize with no symptoms
Complications: otitismedia, sinusitis, or rarely arthritis, endocarditis, meningitis
A

• “Strep Throat”group A

59
Q
  • Most common causeofneonatal pneumonia, meningitis, sepsis
  • Fatal in 3-4%ofneonates
  • Normal vaginal flora in 30% females
  • may be passed on to baby as it passes through birth canal
  • Only 1%ofthese babies developinfection
  • Infectionin baby: hypotension, pneumonia,bacteremia, meningitis
  • Thisisthe reason moms are put on antibiotics just before delivery due date
A

Streptococcus agalactiae Group B

60
Q

• Inflammationofa lymph vessel

A

• Lymphangitis”angi” = vessel

61
Q

• Know traumatic skin injuries

A

Mechanical trauma
• Minor trauma doe not even register while major trauma may have serious consequences

• Major trauma usually is not limited to the skin alone but involves others organs as well and may be lethal

62
Q

– well-differentiated, closely resembling tissue of origin; slow growth, usually encapsulated; no metastasis (suffix = oma)

A

• Benign tumor

63
Q

increase in size

A

■ Hypertrophy:

64
Q

– lack capsule, capable of invasion into adjacent structures and metastasis

A

• Malignant tumor (cancer)

65
Q

Develop on the skin overlying a bone pressing on a firm external surface

A
  • Pressure Ulcers (Decubitus ulcers or Bed sores) •
  • More common in hospitalized patients (spinal cord or cerebral trauma or strokes)
  • Other factors include circulatory disturbances, poor nutrition, sensory deficits, friction, moisture
66
Q

• May be caused by short exposure to very high or very ow temperatures or by prolonged exposure to moderately high or low temperatures

A

• Thermal injury

67
Q
  • caused by heat
  • Severity depends on mode of exposure, duration of exposure, the temperature and the anatomic site of injury
  • Clinical outcome depends on the depth of the skin injury and the extent of the body surface affected
A

Burns

68
Q

• Frostbite and immersion foot injury

A

(Trench foot) • Cold injury

69
Q

• Due to contact with unprotected and inadequately isolated electrical wires, lightening

A

• Electrical injury

70
Q

• Caused by Sunlight and ionizing radiation

A

• Radiation injury

71
Q

• Inflammationofone or more lymph nodes

A

• Lymphadenitis”aden” = gland

72
Q

• Increased lymph fluid in the tissues

A

• Lymphedema “ederna” = swelling

73
Q

• Enlargementofthe lymph nodes

A

• Lymphadenopathy

74
Q

cellis transforming in to diff shape

A

■ Metaplasia: (meta = change)

75
Q

increase in sizeandnumber ofcells

A

■ Hyperplasia:

76
Q

– is a chronic nail infection

A

• Tinea unguium

77
Q

– presents on the skin and appear as circular or irregular shaped patches

A

• Tinea corporis

78
Q
  • affects the groin region
A

• Tinea cruris or jock itch

79
Q

– typically affects children and cause local hair loss

A

• Tinea capitis or scalp ringworm

80
Q

-a condition in which red blood cells are destroyed and removed from the bloodstream before their normal lifespan is up
◦ RBC antigens of these patients become antigenic and are recognized as foreign by the body’s own immune system

A

Type II: cytotoxic antibody mediated

o Hemolytic anemia

81
Q

 instead of being cleared by the body, they deposit in tissues around small blood vessels

A

Type III: immune complex mediated
− Vasculitis Ag-Ab complex formation
This leads to vasculitis ◦ inflammation of a blood vessel or blood vessels

Vasculitis leads to: ◦ Wheals (inflammation of skin) ◦ Synovitis (inflammation of joints)
Ex. RA ◦ Nephritis (inflammation of kidneys)
◦ Pleuritis (inflammation of pleura surrounding lungs)
◦ Pericarditis (inflammation of pericardium)

82
Q

o Sarcoidosis-◦ idiopathic granulomatous disease
◦ most commonly the lungs, lymph nodes, eyes and skin.

o Contact dermatitis -Does not include granuloma but skin contains infiltrates of T cells and macrophages Examples:  latex, poison ivy, “gold” rings containing Nickel

A

Type IV: cell mediated, delayed hypersensitivity reaction

83
Q

mature in bone marrow
• Differentiate into immunoglobulin producingplasmacellsor memory BCells
• Part of Humoral Immunity

A

B Lymphocytes

  • Memory B-cells
  • circulate among the blood, lymphoid system,andtissues for 1 year or longer
  • responsible for more rapidandsustained immune response that occurs with repeated exposure to the same antigen

• Plasmacells
• Fully differentiated B lymphocytes
• Produce immunoglobulins (antibodies) (Ig)
• Surface ofplasmacell is coated with Ig
5 types of antibodies produced

84
Q

• Gram positive bacteria
• Spread through aerosol or skin shedding’s
Range from asymptomatic carriage to life-threatening syndrome that includes pharyngitisand toxin-mediated damage to heart, nerves, and other organ

A

Corynebacterium Diphtheria(group B)

85
Q

– aerobic gram negative
• opportunistic pathogen, spread by contact
• Most common nosocomial pathogens Seen in hospitals
• Uncommon in healthy populations
• Thrives in pools, tubs (moist environ.)
• Pneumonia, woundinfections esp. Burns, sepsis, UTIs, osteochondritis
• Inherently antibiotic-resistant

A

Pseudomonas(group B)

• P. aeruginosa

86
Q

isa Gram-negative,rod shapedcoccobacillus, a facultative anaerobic bacterium that can infect humans and animals.
• It causes the deadly disease named plague

A

Yersinia pestis(group B)

87
Q

• Gram-negativecoffee bean-shapeddiplococci aerobic bacteria

A

NeisserialInfections(Group B)

• Neisseria gonorrhoeae (gonococcus) -responsible for the sexually transmittedinfectiongonorrhea

• Neisseria meningitides (meningococcus) – significant causeofbacterial meningitis

88
Q

isa very important gram + organism because itisamajor causeofbacterial pneumonia and meningitisin adults, and otitismedia in children

• Etiology& Risk Factors
• post-influenza or viral URTI, chronicdisease,immunosuppression, alcohol abuse

A

Streptococcus pneumoniae
• The pneumococcus(group B

• Clinical FeaturesofStrep Pneumoniae pneumonia:
• acute fever, chills
• pleuritisw/ pleuritic chest pain
• Dyspnea
• productive cough or purulent sputum - possibly blood-streaked

89
Q

Gram +
• gas gangrene
• Etiology: severe trauma, wartime injury, septic abortion
• Pathogenesis:
• deathoftissue with lossofvasculature, bacterial invasion, fermentation gas and putrefaction (decomposition)
• Clinical Features: <3 days after injury sudden severe pain
• discharge with foul
• odour
• Prognosis: possibly amputation, extremities better than visceral or trunk

A

Clostridium(group B)

• ClostridiumPerfringes

90
Q 
• Usually follows untreated Strep throat
• pyogenic exotoxinisreleased
• Kids ages 2-10
• Clinical Manifestations:
• Sore throat,
• fever,
• strawberry tongue,
• Rash which starts on upper chest, spares palms/soles
Desquamationofpalms and soles later on
A

Scarlet Fever Group A

91
Q
  • Seriousinfectionthat progresses rapidly along fascial planes
  • Usually in legs
  • Causes severe tissue damage
  • Used to be called Streptococcal gangrene
  • Edema, tenderness, pain, fever
A

Necrotizing FasciitisGroup A

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