systemic pathology 400 (CV class 4) Flashcards

1
Q

telangiectasis

A

aka “ spider veins”

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

what are spider veins (telangiectasia)

A

Vascular lesion formed by dilation of a group of small blood vessels

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

where can spider veins occur? whre are they most common

A

Can occur anywhere on the skin

Most frequently seen on the face and thighs

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

is spider veins a serious issue

A

generally just a cosmetic condition –> generally no functional effect on health

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

how can spider veins appear?

spider veins vs childhood

A

May appear as a birthmark or become apparent in young children

“Spider telangiectasias are fairly common and look like little red lines on a child’s skin. They are usually nothing more than a cosmetic problem. They form as a result of abnormal blood vessels (a.k.a. a vascular anomaly). Spider telangiectasias don’t cause any health problems.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

risk factors / associated factors (telangiectasis)

A

May be associated with

long term sun exposure,
standing,
age,
varicose veins,
gender,
pregnancy,
trauma,
steroid treatment,
rosacea, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

telangiecstasis etymology

A

telos = end

angeion = vessel

ektasis = dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

frostbite

A

Localized medical condition whereby damage is caused to skin and other tissues due to extreme cold.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

frostbite – etiology / risk factors

A

Extreme cold/wind chill
Wet clothes
Poor circulation
Blood vessel d/o
Low body fat
Age
Medications
Smoking, alcohol, drugs
Homelessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

frostbite – pathogenesis

A

Vasoconstriction upon exposure to cold

—> This helps to preserve core body temperature

Ice crystals form in tissues and expand into extracellular spaces
—> cell membrane rupture
—> disruption of enzyme activity
—> tissue death

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

retrostasis vs hunting response

A

retrostasis at first

hunting response after 10-15 or 20 (?) minutes
—> alternating vasodilation/constriction to prevent superficial tissue damage

when cold continue however, – body goes back to RETROSTASIS –> b/c the vital organs need to maintain temperature to prevent death

—> thus superficial tissue loses blood supply, and can die d/t anoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

frostbite classification

(superficial classification)

A

Superficial frostbite affects skin and subcutaneous tissue

—> Discoloration of the skin, burning and/or tingling, swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

(deep frostbite)

A

Deep frostbite extends beyond the superficial tissue

—> White skin, pain, blisters, tissue necrosis, gangrene

—> ultimately turns black (?) when dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

frostbite Dx

A

Based on history and clinical presentation

Bone scan

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

frostbite and bone scan

A

if frostbite/necrosis has reached bone –> then amputation must take place

“It is concluded that scintigraphy is an excellent means of evaluating patients with severe frostbite of the extremities: as early as day 2 after the injury it can indicate whether amputation is necessary, and between days 2 and 8 it provides valuable information on the efficacy of treatment.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

scintigraphy

A

a technique in which a scintillation counter or similar detector is used with a radioactive tracer to obtain an image of a bodily organ or a record of its functioning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

frostbite tx

A

Vasodilators

Rewarm the area without rubbing or massaging
—> Reperfusion injury is a serious complication

Pain meds

Surgery, amputation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

reperfusion ?

A

“Reperfusion is the restoration of blood flow to an organ or tissue after having been blocked, and may refer to: Reperfusion injury, tissue damage caused when blood supply returns to the tissue.

Reperfusion therapy, the medical treatment that restores blood flow through blocked arteries, typically after a heart attack.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why does reperfusion cause tissue damage

A

The inflammatory response is partially responsible for the damage of reperfusion injury. White blood cells, carried to the area by the newly returning blood, release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

diabetic microangiopathy

A

Years of poorly controlled hyperglycemia leads to vascular complications that affect small (microvascular) vessels, large (macrovascular) vessels, or both.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

pathogenesis (diabetic microangiopathy)

A

Vascular disease due to:

Glycosylation of serum and tissue proteins

Superoxide production

Activation of signaling molecules
—> increase vascular permeability
—> endothelial dysfunction

Hypertension

Arterial microthromboses

Hyperglycemia/hyperinsulinemia
—> inflammation and prothrombotic effects
—> impaired vascular autoregulation

Hyperglycemia
—> impaired cellular immunity
—> immune dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

glycoxidation

A

“Glycoxidation is a process whereby glycated proteins chemically generate oxygen free radicals.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

why superoxide production

A

However, in diabetic conditions, the uncoupling of eNOS in diabetic vascular endothelial cells leads to the overproduction of superoxide anion (O2* −), which decreases NO availability, impairs the endothelium and ultimately increases superoxide in blood vessels [23].

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

1) diabetic microangiopathy VS Diabetic retinopathy

A

No early symptoms or signs, but blurring, retinal detachment, and partial or total vision loss eventually develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

diabetic retinopathy is…

A

Most common cause of adult blindness in the US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

2) diabetic microangiopathy vs Diabetic neuropathy

A

The result of nerve ischemia from microvascular disease, direct effects of hyperglycemia on neurons, and intracellular metabolic changes that impair nerve function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

diabetic retinopathy pathogenesis (?)

A

The pathologic process involved in DME is the resultant fluid leaking into the retina and depositing under the macula. Sediment left behind from this edema leads to waxy, yellow lipid byproducts referred to as hard exudates.

(Diabetic macular edema (DME))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

diabetic nephropathy

A

Involves glomerular sclerosis and fibrosis caused by the metabolic and hemodynamic changes of diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

diabetic nephropathy is

A

The number one cause of renal failure in the US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

note about diabetic neuropathy (as a result of diabetic microangiopathy)

A

also recall CHARCOT’S neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

decompression sickness

A

AKA caisson disease, the bends, divers disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is decompression sickness?

A

Decompression sickness occurs when rapid pressure reduction (e.g. during ascent from a dive, or ascent to altitude) causes gas previously dissolved in blood or tissues to form bubbles in blood vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

decompression sickness and Henry’s law

A

The solubility of a gas in a liquid is directly proportional to the pressure exerted on the gas and liquid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

steps during decompression sickness

A

during descent (diving)
—> nitrogen moves from high pressure in lungs too blood (low pressure)

swimming up too quickly doesn’t give nitrogen enough time to leave blood
—> forms bubbles that lead to SSx

whereas a slow ascent would let the nitrogen gradually return to lungs where it is breathed out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

decompression sickness – incidence

A

Approximately 2 to 4/10,000 dives

Men > women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

decompression sickness – RISK FACTORS

A

Cold temperature dives
Prolonged or deep dives
Rapid ascent
Dehydration
Flying after diving
Obesity
Older age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

why is it called the bends?

A

DCS often causes air bubbles to settle in major joints like knees or elbows, causing individuals to bend over in excruciating pain, hence its common name, the bends.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

caisson

A

a large watertight chamber, open at the bottom, from which the water is kept out by air pressure and in which construction work may be carried out under water.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

why called caisson disease

A

The original name for DCS was “caisson disease”. This term was introduced in the 19th century, when caissons under pressure were used to keep water from flooding large engineering excavations below the water table, such as bridge supports and tunnels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

decompression sickness SSx

A

Dependent on which tissue is affected:

Joint and muscle pain
N/V
dyspnea (shortness of breath)
Numbness, tingling, formication
Seizures
Itching and/or rash
Hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

formication define

A

Formication is a symptom where you hallucinate the feeling of insects crawling in, on or under your skin. This symptom can be very upsetting or disturbing, leading to other issues like self-injury from scratching or trying to get the insects out from under or inside of your skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

decompression sickness – dx, tx

A

Diagnosis
History and clinical manifestation

Treatment
Oxygen chamber and recompression therapy

43
Q

decompression sickness – px

A

Prognosis
About 80% of patients recover completely

20% may have long term / chronic SSx

44
Q

varicose veins aka

A

AKA varicosities

45
Q

what are varicose veins?

A

An abnormal dilation of veins leading to tortuosity (twisting and turning) of the vessel,

incompetence of the valves, and a propensity to thrombosis

46
Q

varicose veins incidence

A

Women are affected more often than men (secondary to pregnancy) until 70 y.o.

70% of women ages 60-70 have varicose veins

Usually develops between ages 30-50

47
Q

varicose veins risk factors

A

Periods of high venous pressure associated with:

Heavy lifting
Prolonged sitting or standing
Hormonal changes
Menopause
Pregnancy
Heart failure
Constipation (hemorrhoids)
Hereditary factors*
CT disease
Valvular incompetence
Obesity

48
Q

varicose veins common sites

A

Lower extremity

Saphenous vein

Rectum and anal canal – hemorrhoids (can be internal or external)

Scrotum - varicocele

49
Q

varicocele risk factors

A

age
genetics
anatomy
testicular growth
physical exertion
sedentary lifestyle
occupation
body weight
heat exposure
infertility

50
Q

varicose veins genreally @

A

superficial veins

51
Q

varicose veins – clinical manifestations

A

The clinical picture is not correlated with the severity of the varicosities

The development of varicose veins is gradual.

Most are asymptomatic (perhaps with the exception of hemorrhoids)

52
Q

most common symptom of varicose veins (when symptomatic)

A

The most common symptom is dull, aching heaviness, tension, or fatigue brought on by standing.

53
Q

varicose veins of scrotum (varicocele)

A

could be d/t serous fluid production in scrotum

54
Q

“The clinical picture is not correlated with the severity of the varicosities”

A

I.e. a tiny varicosity could be painful and achy

& large amounts of varicosities could be asymptomatic

(Recall, similar to osteoarthritis – amount of wear/damage does not necessarily correlate to SSx/pain)

55
Q

varicose veins – other notes about clinical manifestations

A

Clinical Manifestation:

Cramps are relieved with elevation of legs

Itching may occur

The veins are dilated, tortuous and elongated beneath the skin

56
Q

secondary changes of varicose veins

A

Secondary changes include browning and swelling

Veins may become thick and hard to the touch

57
Q

varicose veins – complicaitons

A

Ulcers due to compromised circulation

Thrombosis

Inflammation of the vein - phlebitis

58
Q

how can varicose veins lead to phlebitis

A

A common pathway for developing phlebitis is when a clot develops in a varicose vein, just underneath the skin surface.

Symptoms of phlebitis are caused by inflammation, which represents the body’s response to injury or tissue damage.

Phlebitis can be triggered by excessive stretching of the leg veins.

59
Q

venous thrombosis

A

..

60
Q

venous thrombosis define

A

Venous thrombosis - partial or full occlusion of a vein by a clot

61
Q

phlebothrombitis

A

inflammation of a vein, predisposing a person to clot formation

(also note form previous card – clot can lead to inflammation, and inflammation can lead to clot (?)

62
Q

thrombophlebitis

A

partial or complete occlusion of a vein by a thrombus (clot) with a secondary inflammatory reaction in the wall of the vein

63
Q

thrombophlebitis vs phlebothrombitis

A

“Thrombophlebitis is a condition in which inflammation of the vein wall has preceded the formation of a thrombus (blood clot). Phlebothrombosis is the presence of a clot within a vein, unassociated with inflammation of the wall of the vein (Fig. 27.6).”

—> NOTES DIFFERENT = inflammation is risk factor for the clot

vs above: “clot within a vein, unassociated with inflammation of the wall”

64
Q

venous thrombosis – Classificaiotn

A

superficial vs deep

65
Q

deep venous thrombosis

A

Deep (DVT)

Usually present in the calf.

It is often clinically silent and benign although complications can lead to pulmonary emboli.

Thromboses in the popliteal, femoral, iliac veins or inferior vena cava are associated with greater risk of PULMONARY EMBOLISM

66
Q

which DVT locaitons are risk factors for pulmonary embolism

A

popliteal,
femoral,
iliac veins
or inferior vena cava

67
Q

venous thrombosis – etiology and risk factors

A

Surgery – most common
Genetics

Oral contraceptives
Smoking
Venous stasis
Hypercoagulability of blood

68
Q

venous thrombosis – incidence

A

DVT is the third most common CV disease after coronary artery episodes (heart attack) and cerebrovascular accidents (stroke).

2 million Americans die of DVT per year

69
Q

DVT mechanism of death

A

Deep vein thrombosis can be serious because blood clots in the veins can break loose. The clots can then travel through the bloodstream and get stuck in the lungs, blocking blood flow (pulmonary embolism). When DVT and pulmonary embolism occur together, it’s called venous thromboembolism (VTE).

70
Q

venous thrombosis pathogenesis

A

Trauma to endothelium of the vein exposes subendothelial tissue to platelets and clotting factors, initiating thrombosis

Platelets adhering to vessel wall attract fibrin, leukocytes, erythrocytes

Clot can undergo recanalization, dissolution, organization, or can persist as a thrombus or break free and become an embolus

71
Q

venous thrombosis – clinical manifestation

A

Variable and inconsistent

Asymptomatic

LE>UE

Edema

Dull ache

Tightness, tenderness

Swelling

72
Q

venous thrombosis Dx

A

Based on signs, symptoms
and risk factors

Ultrasound

73
Q

venous thrombosis – Tx

A

Elastic stockings (COMPRESSION SOCKS)

Medications

Surgery

74
Q

why do compression socks help with venous thrombosis?

A

Compression socks, which are made from synthetic materials, are tighter than regular socks.

They apply controlled pressure to improve blood flow in the veins of the leg. There are medical-grade compression stockings that are “graduated”—tightest at the ankles, with the compression gradually easing up the legs.

“The compression of the socks gently pushes blood flow up the leg, helping to prevent swelling and even blood clots.”

75
Q

venous stasis

A

AKA postphlebitis syndrome, chronic venous insufficiency

76
Q

postphlebitis syndrome vs post-thrombotic syndrome

A

Post-thrombotic syndrome refers to symptoms and signs of chronic venous insufficiency that develop following deep vein thrombosis (DVT) and is a common, burdensome, and costly complication [1,2].

The term “post-thrombotic” replaces the prior terminology “postphlebitic” syndrome

**

“Immediate compression and walking seems also to reduce the incidence of a postthrombotic syndrome.” (w/ respect to compression socks and venous thrombosis)

77
Q

so what is venous stasis?

A

Inadequate venous return over a long period of time

78
Q

VENOUS STASIS – two relevant risk factors

A

venous thrombosis

and varicose veins

79
Q

venous stasis and venous thrombosis

A

Venous stasis syndrome is typically considered a long-term sequel of deep vein thrombosis (DVT; also known as post-thrombotic syndrome or post-phlebitic syndrome in the post-DVT setting). The cumulative incidence of venous stasis syndrome after DVT is 20–50%, with a third being severe venous stasis syndrome4–9.

Note:
that’s why venous stasis is aka post-thrombotic synrome

80
Q

venous stasis and varicose veins

A

Conclusions. Increasing patient age and BMI, prior DVT (particularly left leg DVT), longer time interval since DVT and varicose veins are independent risk factors for venous stasis syndrome.

81
Q

venous stasis typically follows…

A

Follows most severe cases of DVT

82
Q

venous stasis can also occur secondary to

A

varicose veins,
leg trauma,
or neoplasms

83
Q

venous stasis – clinical manifestations

A

Progressive edema of the leg

Thickening, coarsening, and brownish pigmentation of the skin around the ankles (stasis dermatitis)

Venous stasis ulceration
—> Painful, shallow wounds
—> Large amounts of drainage

84
Q

stasis dermatitis (note individuals with brown ankles)

A

Stasis dermatitis involves skin changes that are caused by poor circulation and the resulting pooling of blood in the lower legs. Also called gravitational dermatitis and venous eczema, this condition could develop with aging, but it could also indicate the presence of another condition, like kidney or heart disease.

85
Q

venous stasis – Dx & Tx

A

Diagnosis:
History and examination

Treatment:
Treatment is as for varicose veins.

Prognosis:
Poor

86
Q

Treatment:
Treatment is as for varicose veins.

A

Rest and elevation

Exercise

Elastic stockings (COMPRESSION SOCKS)

Surgery, if necessary

87
Q

venous stasis aka

A

chronic venous insufficiency

88
Q

Raynaud’s

A

Raynaud’s disease: Occurs on its own and isn’t connected with another disease or condition. This is also called primary Raynaud’s syndrome.

Raynaud’s phenomenon: Occurs due to an underlying condition, medication or lifestyle factor. This is also called secondary Raynaud’s syndrome.

Raynaud’s syndrome: Refers to either the primary or secondary form of the condition.

89
Q

Raynaud’s is

A

Intermittent episodes of small artery or arteriole constriction of the extremities causing temporary pallor and cyanosis of the digits and changes in skin temperature

90
Q

why does Raynaud’s take place

A

Occurs in response to cold temperature, anxiety or excitement

91
Q

Primary Vasospastic Disorder (Raynaud’s Disease)

A

Idiopathic

92
Q

Raynaud’s Phenomenon

A

Secondary to another disease or underlying cause

93
Q

RAYNAUD’S – incidence / risk factors

A

Usually more common in women

Age

Smoking, alcohol may be a factor.

94
Q

Raynaud’s can also be associated with

A

occlusive arterial disease,

neurogenic lesions,

TOS,

frostbite,

trauma,
the chronic use of vibrating equipment,
repetitive stress

injuries to the small vessels of the hands,

95
Q

vibration Raynaud’s

A

Vibration white finger is a type of secondary Raynaud’s phenomenon. In this type, blood vessels, nerves, and other tissue become damaged due to chronic vibration.

96
Q

also a known risk factor

A

Possibly a disturbance in the control of vascular reflexes

—> overactive sympathetic nervous system in that area —> vasoconstriction

97
Q

Raynaud’s clinical manifestation

A

White, blue, then red digits

—> MORE OFTEN IN UE than LE

Throbbing, paresthesia, swelling

—> Sensory changes, such as numbness, stiffness, diminished sensation, aching pain often occur.

98
Q

what can prolonged Raynaud’s do to hands/fingers

A

Over time, frequent prolonged episodes can cause the fingertips to thicken and the fingernails to become brittle.

99
Q

Raynaud’s typical phases

A

phase 1: Ischemia

phase 2: Cyanosis

phase 3: Rubor

100
Q

Raynaud’s Dx

A

Diagnosis based on clinical presentation and history

101
Q

Raynaud’s disease (primary Raynaud’s) Dx

A

Raynaud’s disease – history of symptoms for at least 2 years with no progression and no evidence of underlying cause

(idiopathic)

102
Q

Raynaud’s Tx

A

Avoid triggers

Decrease smoking

Physical therapy

Relaxation techniques

Exercise

Heat

103
Q

Raynaud’s Px

A

Untreated and uncontrolled Raynaud’s may damage or destroy affected digits. (long term)

Disability and loss of function can occur.

RECALL:
“Over time, frequent prolonged episodes can cause the fingertips to thicken and the fingernails to become brittle. “

104
Q
A