Patho Acne/Psor/Gout/Glau Flashcards

Pathology of Ance, Psoriasis, Gout and Glaucoma

1
Q

Glaucoma

A
  • Elevated Intraocular Pressure THAT RESULT IN DAMAGE TO THE OPTIC NERVE OFTEN LEADING TO LOSS OF SIGHT
  • LOSS OF VISIONIS PERMANENT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Glaucoma Classification

A
  • Closed-angle
  • Open-angle
  • Congenital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Closed-Angle Glaucoma

A
  • FLUID DRAINAGE FROM THE EYE IS BLOCKED
  • THIS FORM CAN PRESENT GRADUALLY OR SUDDENLY
  • INVOLVES SEVERE EYE PAIN
  • BLURRED VISION
  • MID-DIALTED PUPIL
  • REDNESS OF THE EYE
  • NAUSEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Open-Angle Glaucoma

A
  • THE DRAINAGE FROM THE EYE REMAINS OPEN
  • DEVELOPS SLOWLY
  • NOT ASSOCIATED WITH PAIN
  • GRADUAL LOSS OF PERIPHERAL VISION
  • CENTRAL VISION LOSS DEVELOPS WITH LOSS OF VISION
  • MAJORITY OF THE CASES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Congenital Glaucoma (infantile)

A
  • CAUSE IS OBSTRUCTION OT AQUEOUS DRAINAGE DUE TO DEVELOPMENTAL ANOMALIES
  • 65% OCCUR IN BOYS IN AN X-LINKED RECESSIVE MODE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glaucoma

Risk Factors

A
  • FAMILY HISTORY OF THE CONDITION
  • HIGH BLOOD PRESSURE
  • INCREASE PRESSURE IN THE EYE (OCULAR HYPERTENSION)
  • CONGENITAL MALFORMATION
  • EAST ASIAN ANCESTRY
  • MUTATED GENES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Patho

Open-Angle

A
  • REDUCED FLOW DUE TO DEGENERATION AND/OR OBSTRUCTION OF THE TRABECULAR MESHWORK
  • REDUCTION IN TRABECULAR FLOW CAUSES AN INCREASE IN PRESSURE AS THE CILIARY PROCESS CONTINUES TO PRODUCE AQUEOUS HUMOR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Patho

Closed-Angle

A
  • THE CHANNEL BETWEEN THE ANTERIOR AND POSTERIOR IS COMPLETELY CLOSED
  • CAUSED BY DISPLACEMENT OF THE IRIS AGAINST THE CORNEA
  • ACCUMULATION OF AQUEOUS HUMOR CAUSE ACUTE INCREASE IN PRESSURE AND PAIN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effects of increased ocular pressure

A
  • INCREASED INTRAOCULAR PRESSURE LEADS TO CUPPED EXCAVATION OF THE OPTIC NERVE HEAD
  • THE CORNEA OR SCLERA BULGES AT WEEK POINTS
  • OPTIC NERVE ATROPHY WITH LOSS OF AXONS, GLIOSIS AND THICKENING OF THE PIAL SEPTA
  • VISION DECLINES WITH LOSS OF NEURONS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Gout

Causes

A

GOUT IS DUE TO PERSISTENT ELEVATED LEVELS OF URIC ACID IN THE BLOOD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Gout

Underlying causes

A
  • GENETIC FACTORS (60%)
  • DIET (12%)
  • OTHER HEALTH PROBLEMS (COMORBIDITY)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gout

A
  • a form of arthritis
  • typically at the base joint of the big toe is affected
  • may lead to the formation of kidney stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gout

Characterization

A
  • RECURRENT ATTACKS
  • RED,TENDER, HOT,
  • SWOLLEN AND PAINFUL JOINTS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diet and Gout

A

Associated with foods high in purine
* MEAT
* SEAFOOD
* ALCOHOL
* MUSHROOMS
* BEER YEAST
* SEAWEED

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

Patho of Gout

A
  1. HIGH BLOOD LEVELS OF URIC ACID CAUSE URIC ACID TO
    CRYSTALLIZE
  2. SUCH CRYSTALS THEN DEPOSIT IN JOINTS, TENDONS AND
    SURROUNDING TISSUES
  3. SOMETIMES BLOOD URIC ACID LEVELS ARE NORMAL DURING
    BLOOD WHILE DEPOSITS ARE FOUND IN THE JOINTS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gout

Two mechanism for High Uric acid

A
  • UNDEREXCRETION OF URIC ACID BY THE KIDNEY (90%)
  • OVERPRODUCTION OF URIC ACID (10%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Disorder of Purine Metabolism

A
  • CRYSTAL OF URIC ACID FORM AS MONOSODIUM URATE
  • URATES PRECIPITATE IN TISSUES
  • TOPHI MAY BE WALLED OFF BY A RING OF PROTEINS THAT BLOCK OFFINTERACTION OF CRYSTALS WITH CELL
  • URATE CRYSTALS MAY LEAK FROM TOPHI UNDER PHYSICAL
    STRESS
  • LEAKED CRYSTALS THEN TRIGGER A LOCAL IMMUNE-MEDIATED INFLAMMATORY REACTION IN MACROPHAGES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NLRP3 INFLAMMASOME
PROTEIN COMPLEX

A
  • Initiates Inflammation
  • recruits Caspase 1 enzyme
19
Q

Caspase 1

A
  • Converts pro-interleukin 1B into active IL-1B
  • Important for inflammatory cascade
20
Q

Gout

Anatomical changes

A
  • SUBDERMAL NODULES MAY FORM: VARY IN SIZE
  • TOPHI MAY FORM FROM CRYSTALS OF URIC ACID SURROUNDED BY CELLULAR ELEMENTS – OFTEN HISTOCYTES
21
Q

Leakage of Crystals from Tophi

A
  • bone erosion
  • cartilage damage
22
Q

Chronic kidney disease and Gout

A
  • NEPHRON FAILS TO FILTER OUT URIC ACID WASTE
  • SUCH FAILURE LEADS TO A BUILD UP OF URIC ACID IN THE BODY
23
Q

Gout cause Kidney failure

A
  • HIGH BLOOD URIC ACID CAN PRODUCE A KIDNEY FILTRATE HIGH IN URIC ACID.
  • SUCH URATE MAY PRECIPATE IN THE RENAL TUBULE AND PHYSICALLY DAMAGE THE NEPHRON
  • THE ON-GOING PROCESS OF NEPHON FAILURE LEADS TO CHRONIC RENAL FAILURE
24
Q

Psoriasis

A
  • DISORDER OF THE SKIN CHARACTERIZED BY RAISED AREAS OF ABNORMAL TISSUE THAT IS AUTOIMMUNE IN NATURE.
  • TYPICALLY THE SKIN IS RED TO PURPLE, DRY, RAISED, AND ITCHY
25
Q

Types of Psoriasis

A
  • PLAQUE
  • GUTTATE
  • INVERSE
  • PUSTULAR
  • ERYTHRODERMIC
26
Q

Plaque Psoriasis

A
  • TYPICALLY 90% OF CASES
  • PRESENTS AS RED PATCHES WITH WHITE SCALES ON TOP
27
Q

Guttate Psoriasis

A
  • NUMEROUS SMALL SCALY RED OR PINK PAPULES
  • DROP-SHAPED LESIONS
  • SPREAD OVER LARGE AREAS OF THE BODY:
  • PRIMARILY THE TRUNK, LIMBS AND SCALP
  • LESIONS ARE OFTEN TRIGGERED BY STREPTOCOCCAL NFECTONS
28
Q

Pustular Psoriasis

A
  • PRESENTS AS SMALL NON-INFECTIOUS, PUS-FILLED BLISTERS
  • SKIN UNDER THE PUSTULES IS USUALLY RED AND TENDER
  • PUSTULES MAY BE LOCALIZED OR WIDESPREAD
29
Q

Inverse Psoriasis

A
  • FORMS RED PATCHES IN SKIN FOLDS
  • PATCHES ARE SMOOTH AND INFLAMED
30
Q

Erthrodermic Psoriasis

A
  • WIDESPREAD FORM OF THE DISORDER THAT MAY ARISE FROM ANY OF THE OTHER TYPES. – OFTEN 90% OF BODY SURFACE
  • WIDESPREAD EXFOLIATIONOF THE SKIN
  • OFTEN WITH SEVERE DRYNESS, ITCHING, SWELLING AND PAIN
  • MAY BE FATAL AS THE EXTREME INFLAMMATION AND EXFOLIATION DISRUPTS THE BODY’S ABILITY TO REGULATE TEMPERATURE AND PERFORM BARRIER FUNCTION
31
Q

Sebhorrhic-Like psoriasis

A
  • FORM WITH CLINICAL ASPECTS OF PSORIASIS AND SEBORRHEIC DERMATITIS
  • FORMS RED PLAQUES
  • GREASY SCALES ESPECIALLY IN AREAS SUCH AS SCALP, FOREHEAD, SKIN FOLDS NEXT TO THE NOSE, SKIN AROUND THE MOUTH, ABOVE THE STERNUM AND IN GENERAL SKIN FOLDS
32
Q

Psoriasis in Nails

A
  • PITTING OF NAILS
  • WHITENING OF THE NAISL
  • SMALL AREAS OF BLEEDING FROM CAPILLARIES UNDER THE NAILS
  • YELLOW-REDDISH DISCOLORATION OF NAILS
  • THICKENING OF SKIN UNDR THE NAILS
  • LOOSENING AND SEPARATION OF NAIL
  • CRUMBLING OF THE NAIL
33
Q

Psoriatic Arthritis

A
  • A FORM OF CHRONIC INFLAMMATORY ARTHRITIS
  • ASSOCIATED WITH PSORIASIS OF THE SKIN AND NAILS
  • INVOVLES PAINFUL INFLAMMATION OF THE JOINTS AND SURROUNDING CONNECTIVE TISSUE
  • CAN OCCUR IN ANY JOINT – MOST COMMON IN FINGERS AND TOES
  • MAY ALSO AFFECT HIPS, KNEES, SPINE AND SACROILIAC JOINTS
34
Q

Psoriasis

Causes

A
  • NOT CLEARLY UNDERSTOOD
  • AUTOIMMUNITY
  • GENETICS
  • INDIVIDUALS OFTEN HAVE FAMILY HISTORY
35
Q

Patho of Psoriasis

A
  • STARTS WITH THE INITIATION PHASE – MAY BE SKIN TRAUMA, INFECTION OR IN SOME CASES, DRUGS
  • INITIATION PHASE SEEMS TO LEAD TO ACTIVATION OF THE IMMUNE SYSTEM
  • SKIN CELLS ARE REPACED IN 3-5 DAYS (NORMAL IS 28-30) – PROBABLY CAUSED BY PREMATURE MATURATION OF KERATINOCYTES
  • THE MATURATION RATE IS ALTERED BY INITIATION OF INFLAMMATORY CASCADE IN THE DERMIS
  • DNA RELEASED FROM DYING CELLS MAY ACT AS AN INFLAMMATORY STIMULUS
  • DENDRITIC CELLS ARE INCREASED IN PSORIASIS
36
Q

Psoriasis

Patho Appearance

A
  • SKIN IS THICKENED WITH HYPERKERATOSIS AND PARAKERATOSIS
    (PERSISTENCE OF NUCLEI IN CELLS OF THE STRATUM CORNEUM)
  • NUCLEATED LAYERS OF THE THE EPIDERMIS ARE THICKENED
    SEVERALFOLD
  • IN CHRONIC LESIONS DERMAL PAPILLAE MAY APPEAR AS BULBS
    INSTEADE AS CONES
  • CAPILLARIES OF THE DERMAL PAPILLAE ARE DILATED AND TORTUOUS
37
Q

Acne vulgaris

A

CHRONIC SKIN DISORDER OF HAIR FOLLICLES THAT OCCURS
DUE TO BLOCKAGE BY SKIN CELLS AND SEBUM

38
Q

Comedome

A
  • clogged hair follicle
  • provides environment for growth of commensal skin bacteria
  • start as microcomedomes
  • enlarged microcomedomes = pimples
39
Q

Pimples

A
  • WHITE HEADS: DEEP MICROCOMEDONE
  • BLACKHEADS: SUPERFICIAL MICROCOMEDONE, OPEN TO AIR, WITH OXIDATION OF MELANIN
40
Q

Acne

Risk Factors

A
  • mainly inherited
  • genetic control of androgen production
  • sebum production
41
Q

Acne

Role of Hormones

A

BOTH ANDROGENS AND IGF-1 MAY BE ESSENTIAL FOR THE
DEVELOPMENT OF ACNE, AS ACNE DOES NOT DEVELOP IN
INDIVIDUALS WHO LACK ANDROGEN SENSITIVITY

42
Q

Acne

Role of bacteria and mites

A
  • SPECIFIC SUBSTRAINS OF C. ACNES THAT ARE ASSOCIATED WITH NORMAL SKIN AND OTHER SUBSTRAINS THAT ARE ASSOCIATED WITH ACNE
  • INFECTIONS WITH THE MITE DEMODEX, IS ALSO ASSOCIATED WITH THE FORMATION OF ACNE
43
Q

Acne

Causes of Blocked Hair follicles

A
  • INCREASED SEBUM PRODUCTION
  • EXCESSIVE DEPOSITION OF KERATIN PROTEIN
  • FORMATION OF A COMEDO
  • COLONIZATION OF THE FOLLICLE BY BACTERIA – USUALLY CUTIBACTERIUM ACNES