systemic pathology 400 (CV class 4) Flashcards
telangiectasis
aka “ spider veins”
what are spider veins (telangiectasia)
Vascular lesion formed by dilation of a group of small blood vessels
where can spider veins occur? whre are they most common
Can occur anywhere on the skin
Most frequently seen on the face and thighs
is spider veins a serious issue
generally just a cosmetic condition –> generally no functional effect on health
how can spider veins appear?
spider veins vs childhood
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.”
risk factors / associated factors (telangiectasis)
May be associated with
long term sun exposure,
standing,
age,
varicose veins,
gender,
pregnancy,
trauma,
steroid treatment,
rosacea, etc.
telangiecstasis etymology
telos = end
angeion = vessel
ektasis = dilatation
frostbite
Localized medical condition whereby damage is caused to skin and other tissues due to extreme cold.
frostbite – etiology / risk factors
Extreme cold/wind chill
Wet clothes
Poor circulation
Blood vessel d/o
Low body fat
Age
Medications
Smoking, alcohol, drugs
Homelessness
frostbite – pathogenesis
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
retrostasis vs hunting response
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
frostbite classification
(superficial classification)
Superficial frostbite affects skin and subcutaneous tissue
—> Discoloration of the skin, burning and/or tingling, swelling
(deep frostbite)
Deep frostbite extends beyond the superficial tissue
—> White skin, pain, blisters, tissue necrosis, gangrene
—> ultimately turns black (?) when dead
frostbite Dx
Based on history and clinical presentation
Bone scan
frostbite and bone scan
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.”
scintigraphy
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.
frostbite tx
Vasodilators
Rewarm the area without rubbing or massaging
—> Reperfusion injury is a serious complication
Pain meds
Surgery, amputation
reperfusion ?
“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.”
why does reperfusion cause tissue damage
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.
diabetic microangiopathy
Years of poorly controlled hyperglycemia leads to vascular complications that affect small (microvascular) vessels, large (macrovascular) vessels, or both.
pathogenesis (diabetic microangiopathy)
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
glycoxidation
“Glycoxidation is a process whereby glycated proteins chemically generate oxygen free radicals.”
why superoxide production
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].
1) diabetic microangiopathy VS Diabetic retinopathy
No early symptoms or signs, but blurring, retinal detachment, and partial or total vision loss eventually develop
diabetic retinopathy is…
Most common cause of adult blindness in the US
2) diabetic microangiopathy vs Diabetic neuropathy
The result of nerve ischemia from microvascular disease, direct effects of hyperglycemia on neurons, and intracellular metabolic changes that impair nerve function
diabetic retinopathy pathogenesis (?)
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))
diabetic nephropathy
Involves glomerular sclerosis and fibrosis caused by the metabolic and hemodynamic changes of diabetes
diabetic nephropathy is
The number one cause of renal failure in the US
note about diabetic neuropathy (as a result of diabetic microangiopathy)
also recall CHARCOT’S neuropathy
decompression sickness
AKA caisson disease, the bends, divers disease
what is decompression sickness?
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.
decompression sickness and Henry’s law
The solubility of a gas in a liquid is directly proportional to the pressure exerted on the gas and liquid.
steps during decompression sickness
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
decompression sickness – incidence
Approximately 2 to 4/10,000 dives
Men > women
decompression sickness – RISK FACTORS
Cold temperature dives
Prolonged or deep dives
Rapid ascent
Dehydration
Flying after diving
Obesity
Older age
why is it called the bends?
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.
caisson
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.
why called caisson disease
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.
decompression sickness SSx
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
formication define
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.
decompression sickness – dx, tx
Diagnosis
History and clinical manifestation
Treatment
Oxygen chamber and recompression therapy
decompression sickness – px
Prognosis
About 80% of patients recover completely
20% may have long term / chronic SSx
varicose veins aka
AKA varicosities
what are varicose veins?
An abnormal dilation of veins leading to tortuosity (twisting and turning) of the vessel,
incompetence of the valves, and a propensity to thrombosis
varicose veins incidence
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
varicose veins risk factors
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
varicose veins common sites
Lower extremity
Saphenous vein
Rectum and anal canal – hemorrhoids (can be internal or external)
Scrotum - varicocele
varicocele risk factors
age
genetics
anatomy
testicular growth
physical exertion
sedentary lifestyle
occupation
body weight
heat exposure
infertility
varicose veins genreally @
superficial veins
varicose veins – clinical manifestations
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)
most common symptom of varicose veins (when symptomatic)
The most common symptom is dull, aching heaviness, tension, or fatigue brought on by standing.
varicose veins of scrotum (varicocele)
could be d/t serous fluid production in scrotum
“The clinical picture is not correlated with the severity of the varicosities”
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)
varicose veins – other notes about clinical manifestations
Clinical Manifestation:
Cramps are relieved with elevation of legs
Itching may occur
The veins are dilated, tortuous and elongated beneath the skin
secondary changes of varicose veins
Secondary changes include browning and swelling
Veins may become thick and hard to the touch
varicose veins – complicaitons
Ulcers due to compromised circulation
Thrombosis
Inflammation of the vein - phlebitis
how can varicose veins lead to phlebitis
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.
venous thrombosis
..
venous thrombosis define
Venous thrombosis - partial or full occlusion of a vein by a clot
phlebothrombitis
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 (?)
thrombophlebitis
partial or complete occlusion of a vein by a thrombus (clot) with a secondary inflammatory reaction in the wall of the vein
thrombophlebitis vs phlebothrombitis
“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”
venous thrombosis – Classificaiotn
superficial vs deep
deep venous thrombosis
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
which DVT locaitons are risk factors for pulmonary embolism
popliteal,
femoral,
iliac veins
or inferior vena cava
venous thrombosis – etiology and risk factors
Surgery – most common
Genetics
Oral contraceptives
Smoking
Venous stasis
Hypercoagulability of blood
venous thrombosis – incidence
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
DVT mechanism of death
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).
venous thrombosis pathogenesis
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
venous thrombosis – clinical manifestation
Variable and inconsistent
Asymptomatic
LE>UE
Edema
Dull ache
Tightness, tenderness
Swelling
venous thrombosis Dx
Based on signs, symptoms
and risk factors
Ultrasound
venous thrombosis – Tx
Elastic stockings (COMPRESSION SOCKS)
Medications
Surgery
why do compression socks help with venous thrombosis?
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.”
venous stasis
AKA postphlebitis syndrome, chronic venous insufficiency
postphlebitis syndrome vs post-thrombotic syndrome
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)
so what is venous stasis?
Inadequate venous return over a long period of time
VENOUS STASIS – two relevant risk factors
venous thrombosis
and varicose veins
venous stasis and venous thrombosis
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
venous stasis and varicose veins
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.
venous stasis typically follows…
Follows most severe cases of DVT
venous stasis can also occur secondary to
varicose veins,
leg trauma,
or neoplasms
venous stasis – clinical manifestations
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
stasis dermatitis (note individuals with brown ankles)
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.
venous stasis – Dx & Tx
Diagnosis:
History and examination
Treatment:
Treatment is as for varicose veins.
Prognosis:
Poor
Treatment:
Treatment is as for varicose veins.
Rest and elevation
Exercise
Elastic stockings (COMPRESSION SOCKS)
Surgery, if necessary
venous stasis aka
chronic venous insufficiency
Raynaud’s
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.
Raynaud’s is
Intermittent episodes of small artery or arteriole constriction of the extremities causing temporary pallor and cyanosis of the digits and changes in skin temperature
why does Raynaud’s take place
Occurs in response to cold temperature, anxiety or excitement
Primary Vasospastic Disorder (Raynaud’s Disease)
Idiopathic
Raynaud’s Phenomenon
Secondary to another disease or underlying cause
RAYNAUD’S – incidence / risk factors
Usually more common in women
Age
Smoking, alcohol may be a factor.
Raynaud’s can also be associated with
occlusive arterial disease,
neurogenic lesions,
TOS,
frostbite,
trauma,
the chronic use of vibrating equipment,
repetitive stress
injuries to the small vessels of the hands,
vibration Raynaud’s
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.
also a known risk factor
Possibly a disturbance in the control of vascular reflexes
—> overactive sympathetic nervous system in that area —> vasoconstriction
Raynaud’s clinical manifestation
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.
what can prolonged Raynaud’s do to hands/fingers
Over time, frequent prolonged episodes can cause the fingertips to thicken and the fingernails to become brittle.
Raynaud’s typical phases
phase 1: Ischemia
phase 2: Cyanosis
phase 3: Rubor
Raynaud’s Dx
Diagnosis based on clinical presentation and history
Raynaud’s disease (primary Raynaud’s) Dx
Raynaud’s disease – history of symptoms for at least 2 years with no progression and no evidence of underlying cause
(idiopathic)
Raynaud’s Tx
Avoid triggers
Decrease smoking
Physical therapy
Relaxation techniques
Exercise
Heat
Raynaud’s Px
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. “
