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
2
Q
Glaucoma Classification
A
- Closed-angle
- Open-angle
- Congenital
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
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
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
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
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
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
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
10
Q
Gout
Causes
A
GOUT IS DUE TO PERSISTENT ELEVATED LEVELS OF URIC ACID IN THE BLOOD
11
Q
Gout
Underlying causes
A
- GENETIC FACTORS (60%)
- DIET (12%)
- OTHER HEALTH PROBLEMS (COMORBIDITY)
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
13
Q
Gout
Characterization
A
- RECURRENT ATTACKS
- RED,TENDER, HOT,
- SWOLLEN AND PAINFUL JOINTS
14
Q
Diet and Gout
A
Associated with foods high in purine
* MEAT
* SEAFOOD
* ALCOHOL
* MUSHROOMS
* BEER YEAST
* SEAWEED
15
Q
Patho of Gout
A
- HIGH BLOOD LEVELS OF URIC ACID CAUSE URIC ACID TO
CRYSTALLIZE - SUCH CRYSTALS THEN DEPOSIT IN JOINTS, TENDONS AND
SURROUNDING TISSUES - SOMETIMES BLOOD URIC ACID LEVELS ARE NORMAL DURING
BLOOD WHILE DEPOSITS ARE FOUND IN THE JOINTS
16
Q
Gout
Two mechanism for High Uric acid
A
- UNDEREXCRETION OF URIC ACID BY THE KIDNEY (90%)
- OVERPRODUCTION OF URIC ACID (10%)
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
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
